Dennis M. Mondah presented a seminar topic on multi drug resistant tuberculosis under the guidance of Dr. Prof Ramalingappa, Chairman of the Department of Microbiology at Davangere University. The presentation covered the microbiology, pathogenesis, diagnosis and treatment of tuberculosis, with a focus on drug resistant forms of the disease. It discussed how mutations in genes like inhA, kasA, ndh and rpoB can lead to resistance to first line drugs like isoniazid and rifampicin. Diagnosis of multi drug resistant tuberculosis involves drug susceptibility testing, while treatment follows WHO guidelines using at least four effective drugs over an 18-24 month period. The development of drug resistance poses a challenge for
Objective :
Describe the morphology and structure of mycobacterial tuberculosis ?
What are the tests required for mycobacterial infection :
Mantoux skin test
Sputum examination using Ziehl-Neelsen staining
Sputum culture using lowenstein-jensen media
Discuss the clinical features and transmission of mycobacterial tuberculosis.
What are the pathological changes in mycobacterium tuberculosis?
How to control mycobacterial infection in the environment and vaccine available?
done by : asem shadid , college of medicine .
This document discusses tuberculosis (TB), including its epidemiology, causative agent, pathogenesis, diagnosis, and treatment. Some key points:
- TB is caused by the bacterium Mycobacterium tuberculosis and spreads through airborne droplets when infected individuals cough, sneeze, talk or spit. It can infect the lungs (pulmonary TB) or other organs (extra-pulmonary TB).
- Diagnosis involves microscopic examination of sputum samples for acid-fast bacilli, culture testing, and more recently PCR and gene-based tests. India's Revised National Tuberculosis Control Programme (RNTCP) is based on the WHO DOTS strategy to improve cure rates and case detection.
This document discusses sepsis and provides information on epidemiology, definitions, pathophysiology, and animal models. It notes that sepsis incidence is rising due to aging populations and increased survival of chronic conditions. Sepsis causes over 200,000 deaths per year in the US, often affecting those with pre-existing conditions. The pathophysiology involves an imbalance between pro-inflammatory and anti-inflammatory responses. Common animal models for studying sepsis include administration of toxins like LPS or live bacteria, or disruption of protective barriers through techniques like cecal ligation and puncture.
This document provides information on Mycobacterium tuberculosis and tuberculosis (TB). It begins by defining TB as a chronic infectious disease caused by M. tuberculosis that typically affects the lungs. It then discusses the history of TB, noting it is an ancient disease and one of the leading causes of death worldwide. The document covers topics such as the classification of mycobacteria, morphology and culture of M. tuberculosis, pathogenesis of TB, types of TB infections, and factors that allow secondary TB to develop.
Sirturo (bedaquiline) is a new drug approved by the FDA in 2012 for the treatment of multi-drug resistant tuberculosis. It works by inhibiting mycobacterial ATP synthase, which is essential for energy generation in tuberculosis bacteria. Sirturo represents the first new class of tuberculosis drugs approved in over 40 years. It is meant to be used as part of a combination therapy for drug-resistant tuberculosis when alternative treatment options are limited.
1. Mycobacterium is a genus of bacteria that can cause tuberculosis and leprosy. It has a waxy lipid cell wall and grows slowly.
2. The tuberculosis-causing bacteria include M. tuberculosis, M. bovis, M. africanum, and M. microti. Lepra bacilli that cause leprosy include M. leprae.
3. Diagnosis involves microscopy, culture, nucleic acid tests, tuberculin skin tests, chest x-rays, and analysis of symptoms. Treatment uses several first-line and second-line drugs in combination over 6-8 months to prevent drug resistance.
Dennis M. Mondah presented a seminar topic on multi drug resistant tuberculosis under the guidance of Dr. Prof Ramalingappa, Chairman of the Department of Microbiology at Davangere University. The presentation covered the microbiology, pathogenesis, diagnosis and treatment of tuberculosis, with a focus on drug resistant forms of the disease. It discussed how mutations in genes like inhA, kasA, ndh and rpoB can lead to resistance to first line drugs like isoniazid and rifampicin. Diagnosis of multi drug resistant tuberculosis involves drug susceptibility testing, while treatment follows WHO guidelines using at least four effective drugs over an 18-24 month period. The development of drug resistance poses a challenge for
Objective :
Describe the morphology and structure of mycobacterial tuberculosis ?
What are the tests required for mycobacterial infection :
Mantoux skin test
Sputum examination using Ziehl-Neelsen staining
Sputum culture using lowenstein-jensen media
Discuss the clinical features and transmission of mycobacterial tuberculosis.
What are the pathological changes in mycobacterium tuberculosis?
How to control mycobacterial infection in the environment and vaccine available?
done by : asem shadid , college of medicine .
This document discusses tuberculosis (TB), including its epidemiology, causative agent, pathogenesis, diagnosis, and treatment. Some key points:
- TB is caused by the bacterium Mycobacterium tuberculosis and spreads through airborne droplets when infected individuals cough, sneeze, talk or spit. It can infect the lungs (pulmonary TB) or other organs (extra-pulmonary TB).
- Diagnosis involves microscopic examination of sputum samples for acid-fast bacilli, culture testing, and more recently PCR and gene-based tests. India's Revised National Tuberculosis Control Programme (RNTCP) is based on the WHO DOTS strategy to improve cure rates and case detection.
This document discusses sepsis and provides information on epidemiology, definitions, pathophysiology, and animal models. It notes that sepsis incidence is rising due to aging populations and increased survival of chronic conditions. Sepsis causes over 200,000 deaths per year in the US, often affecting those with pre-existing conditions. The pathophysiology involves an imbalance between pro-inflammatory and anti-inflammatory responses. Common animal models for studying sepsis include administration of toxins like LPS or live bacteria, or disruption of protective barriers through techniques like cecal ligation and puncture.
This document provides information on Mycobacterium tuberculosis and tuberculosis (TB). It begins by defining TB as a chronic infectious disease caused by M. tuberculosis that typically affects the lungs. It then discusses the history of TB, noting it is an ancient disease and one of the leading causes of death worldwide. The document covers topics such as the classification of mycobacteria, morphology and culture of M. tuberculosis, pathogenesis of TB, types of TB infections, and factors that allow secondary TB to develop.
Sirturo (bedaquiline) is a new drug approved by the FDA in 2012 for the treatment of multi-drug resistant tuberculosis. It works by inhibiting mycobacterial ATP synthase, which is essential for energy generation in tuberculosis bacteria. Sirturo represents the first new class of tuberculosis drugs approved in over 40 years. It is meant to be used as part of a combination therapy for drug-resistant tuberculosis when alternative treatment options are limited.
1. Mycobacterium is a genus of bacteria that can cause tuberculosis and leprosy. It has a waxy lipid cell wall and grows slowly.
2. The tuberculosis-causing bacteria include M. tuberculosis, M. bovis, M. africanum, and M. microti. Lepra bacilli that cause leprosy include M. leprae.
3. Diagnosis involves microscopy, culture, nucleic acid tests, tuberculin skin tests, chest x-rays, and analysis of symptoms. Treatment uses several first-line and second-line drugs in combination over 6-8 months to prevent drug resistance.
Anti Tubercular and anti leprotic agents.pdfImtiyaz60
This document provides information on antitubercular agents used to treat tuberculosis. It begins by describing tuberculosis as a chronic infection caused by Mycobacterium tuberculosis that primarily affects the lungs. It is a major global health problem, with over 2 million new cases annually in India alone. The document then discusses the characteristics of M. tuberculosis and the sites it commonly infects in the body. It provides details on first-line and second-line antitubercular drugs, including isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin. It focuses on the mechanisms of action, pharmacokinetics, adverse effects, drug interactions and other important aspects of isoniazid and
Mycobacterium tuberculosis-importance of TB day,classification of Mycobacterium species,Details on Mycobacterium tuberculosis-morphology,culture,resistance,biochemical reactions,antigenic characters,mode of transmission,pathogenesis,complications,lab diagnosis,treatment,DOTS Strategy and prophylaxis
This document provides an overview of mycobacteria, including those of medical importance. It discusses the characteristics of the Mycobacterium genus and important human pathogens such as M. tuberculosis, M. leprae, and M. avium-intracellulare Complex. The pathogenesis and clinical manifestations of tuberculosis are summarized, including the formation of granulomas and typical progression within the lungs. Methods for diagnosis and prevention/control of tuberculosis are also outlined.
M. tuberculosis and M. leprae are acid-fast bacilli that cause tuberculosis and leprosy, respectively. M. tuberculosis was discovered in 1882 and is transmitted through droplets. It has a cell wall containing mycolic acids and is a slow growing obligate aerobe. Laboratory diagnosis involves acid-fast staining of samples from sputum or tissues, as well as culturing on media like LJ. Treatment uses multi-drug therapy including isoniazid and rifampin. M. leprae causes a chronic granulomatous disease affecting skin and nerves. It is not cultivable but can be propagated in animals. Classification systems include tuberculoid, lepromatous, and
1) M. tuberculosis is the bacterium that causes tuberculosis. It is transmitted through airborne droplets when people with active TB cough, sneeze or spit.
2) Symptoms of active TB infection include cough, coughing up blood or sputum, chest pain, weight loss and fever. Latent TB has no symptoms.
3) Diagnosis involves testing sputum samples through microscopy, culture and nucleic acid amplification tests to identify M. tuberculosis bacteria. Chest x-rays are also used.
This document provides information on Mycobacterium tuberculosis, the bacteria that causes tuberculosis (TB). It describes the morphology, cultural characteristics, pathogenesis and symptoms of M. tuberculosis. It also discusses methods of diagnosis like the tuberculin skin test, treatment approaches using combinations of first and second line drugs, and issues of drug resistance like multidrug-resistant (MDR) and extensively drug-resistant (XDR) strains of the bacteria.
This document summarizes information about pulmonary tuberculosis. It begins with definitions of tuberculosis and discusses it being a global public health emergency. It then covers the causes, signs and symptoms, transmission routes, risk factors, stages of infection, and diagnostic steps for tuberculosis. The diagnostic steps include history and clinical examination, radiographic features, and bacteriological evaluation including smear, culture, and new diagnostic methods like MGIT and nucleic acid amplification.
Pulmonary tuberculosis is caused by Mycobacterium tuberculosis, which commonly affects the lungs. The disease is characterized by a cough lasting over 3 weeks, production of sputum, fever, night sweats, and weight loss. Diagnosis involves sputum examination, chest x-rays, and the Mantoux skin test. Treatment involves a combination of antibiotics like isoniazid, rifampin, pyrazinamide, and ethambutol over a period of 6-9 months to prevent development of drug resistance. India has a high burden of tuberculosis with an estimated annual incidence of 1.96 million new cases.
The following presentation is only for quick reference. I would advise you to read the theoretical aspects of the respective topic and then use this presentation for your last minute revision. I hope it helps you..!!
Mayur D. Chauhan
This document provides information about anti-tuberculosis therapy. It begins by listing the learning objectives, which include describing primary and secondary anti-tuberculosis drugs, the phases of TB treatment, mechanisms of action and side effects of drugs, defining multi-drug resistant TB, and the role of vaccines in prevention. It then discusses specifics of TB as a global health problem, treatment regimens, first and second-line drugs, mechanisms of action of isoniazid and rifampin, and side effects of isoniazid. The document aims to educate about best practices for treating TB through use of combination drug therapy.
complete information of tuberculosis including OLD RNTCP and new RNTCP with the novel drug that is marketed; classification of tuberculosis (MDR XDR TDR). special population and tuberculosis treatment clinical presentation and diagnosis
1) TB is caused by Mycobacterium tuberculosis and is one of the top infectious disease killers.
2) It is transmitted through the air and one-third of the world's population is infected with latent TB.
3) Diagnosis involves sputum smear microscopy, culture, tuberculin skin test, chest x-ray and PCR. Treatment requires a minimum of 6 months of multiple antibiotic drugs.
1. Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis that affects the lungs and other organs. It remains a major global health issue, with India accounting for a large number of cases.
2. Treatment involves a combination of antibiotics like isoniazid, rifampin, pyrazinamide, and ethambutol over a period of 6-24 months depending on drug susceptibility and patient category. Directly observed treatment under India's Revised National Tuberculosis Control Programme aims to improve treatment adherence and outcomes.
3. Drug-resistant tuberculosis requires treatment with second-line antibiotics like fluoroquinolones, aminoglycosides, ethionamide, and cycloserine
Mycobacteria are acid-fast rod-shaped bacteria. The most important mycobacteria that cause human disease are Mycobacterium tuberculosis and Mycobacterium leprae, which cause tuberculosis and leprosy, respectively. M. tuberculosis are obligate aerobes that grow slowly over 4-8 weeks on culture medium. They have a cell wall containing waxes and lipids that contribute to their acid-fast staining and ability to evade immune responses. Primary tuberculosis occurs when the bacteria first enter the lungs, while reactivation can occur years later. Diagnosis involves microscopy, culture, or DNA analysis of samples. Treatment requires a multi-drug regimen over several months. M. leprae cannot be cultured but causes
The document discusses Mycobacterium, the genus of bacteria that includes Mycobacterium tuberculosis, which causes tuberculosis. It covers the epidemiology, pathogenesis, diagnosis, and treatment of tuberculosis, noting that it remains a major public health problem, especially in Tanzania where the HIV epidemic has increased the burden of TB. It also discusses other medically important mycobacteria such as Mycobacterium leprae, which causes leprosy.
The document discusses Mycobacterium, the genus of bacteria that includes Mycobacterium tuberculosis which causes tuberculosis. It provides details on the epidemiology of tuberculosis, noting it is one of the top infectious disease burdens globally and in Tanzania specifically. It describes the pathogenesis and clinical presentation of tuberculosis as well as methods for diagnosis and treatment.
Multi Drug Resistance in Tuberculosis Causes and Management Dr Shivansh Verm...shivanshverma55
Multi Drug Resistance in Tuberculosis: Causes and Management
1) Tuberculosis becomes multi-drug resistant when the bacteria develops resistance to both isoniazid and rifampin, the two most effective anti-tuberculosis drugs. 2) Resistance develops through genetic mutations that prevent drugs from binding to their targets in the bacteria. 3) Treatment of multi-drug resistant tuberculosis requires using alternative drugs like fluoroquinolones, cycloserine, para-amino salicylic acid, and injectables that have more adverse effects and toxicity.
This document discusses Mycobacteria and Mycobacterium tuberculosis. It begins by introducing Mycobacteria as acid-fast, aerobic rods. It then discusses the history of discovering M. leprae and M. tuberculosis. Several classifications of Mycobacteria are provided, including M. tuberculosis complex, M. leprae, and non-tuberculous mycobacteria. Extensive details are given on the morphology, pathogenesis, clinical manifestations, diagnosis and treatment of pulmonary and extrapulmonary tuberculosis. Latent tuberculosis and drug-resistant tuberculosis are also summarized.
Mycobacterium are acid-fast, non-motile, non-spore forming bacteria. They include pathogens like M. tuberculosis which causes tuberculosis, M. leprae which causes leprosy, and non-tuberculous mycobacteria (NTM) which can sometimes cause opportunistic infections. M. tuberculosis is transmitted via airborne droplets and causes pulmonary or extrapulmonary infection. Diagnosis involves microscopy, culture, PCR and tuberculin skin testing. Treatment involves a combination of antibiotics over several months. Drug resistant strains like MDR and XDR present a challenge. NTM live in the environment and can cause localized infection, especially in immunocompromised individuals.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
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Anti Tubercular and anti leprotic agents.pdfImtiyaz60
This document provides information on antitubercular agents used to treat tuberculosis. It begins by describing tuberculosis as a chronic infection caused by Mycobacterium tuberculosis that primarily affects the lungs. It is a major global health problem, with over 2 million new cases annually in India alone. The document then discusses the characteristics of M. tuberculosis and the sites it commonly infects in the body. It provides details on first-line and second-line antitubercular drugs, including isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin. It focuses on the mechanisms of action, pharmacokinetics, adverse effects, drug interactions and other important aspects of isoniazid and
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This document provides an overview of mycobacteria, including those of medical importance. It discusses the characteristics of the Mycobacterium genus and important human pathogens such as M. tuberculosis, M. leprae, and M. avium-intracellulare Complex. The pathogenesis and clinical manifestations of tuberculosis are summarized, including the formation of granulomas and typical progression within the lungs. Methods for diagnosis and prevention/control of tuberculosis are also outlined.
M. tuberculosis and M. leprae are acid-fast bacilli that cause tuberculosis and leprosy, respectively. M. tuberculosis was discovered in 1882 and is transmitted through droplets. It has a cell wall containing mycolic acids and is a slow growing obligate aerobe. Laboratory diagnosis involves acid-fast staining of samples from sputum or tissues, as well as culturing on media like LJ. Treatment uses multi-drug therapy including isoniazid and rifampin. M. leprae causes a chronic granulomatous disease affecting skin and nerves. It is not cultivable but can be propagated in animals. Classification systems include tuberculoid, lepromatous, and
1) M. tuberculosis is the bacterium that causes tuberculosis. It is transmitted through airborne droplets when people with active TB cough, sneeze or spit.
2) Symptoms of active TB infection include cough, coughing up blood or sputum, chest pain, weight loss and fever. Latent TB has no symptoms.
3) Diagnosis involves testing sputum samples through microscopy, culture and nucleic acid amplification tests to identify M. tuberculosis bacteria. Chest x-rays are also used.
This document provides information on Mycobacterium tuberculosis, the bacteria that causes tuberculosis (TB). It describes the morphology, cultural characteristics, pathogenesis and symptoms of M. tuberculosis. It also discusses methods of diagnosis like the tuberculin skin test, treatment approaches using combinations of first and second line drugs, and issues of drug resistance like multidrug-resistant (MDR) and extensively drug-resistant (XDR) strains of the bacteria.
This document summarizes information about pulmonary tuberculosis. It begins with definitions of tuberculosis and discusses it being a global public health emergency. It then covers the causes, signs and symptoms, transmission routes, risk factors, stages of infection, and diagnostic steps for tuberculosis. The diagnostic steps include history and clinical examination, radiographic features, and bacteriological evaluation including smear, culture, and new diagnostic methods like MGIT and nucleic acid amplification.
Pulmonary tuberculosis is caused by Mycobacterium tuberculosis, which commonly affects the lungs. The disease is characterized by a cough lasting over 3 weeks, production of sputum, fever, night sweats, and weight loss. Diagnosis involves sputum examination, chest x-rays, and the Mantoux skin test. Treatment involves a combination of antibiotics like isoniazid, rifampin, pyrazinamide, and ethambutol over a period of 6-9 months to prevent development of drug resistance. India has a high burden of tuberculosis with an estimated annual incidence of 1.96 million new cases.
The following presentation is only for quick reference. I would advise you to read the theoretical aspects of the respective topic and then use this presentation for your last minute revision. I hope it helps you..!!
Mayur D. Chauhan
This document provides information about anti-tuberculosis therapy. It begins by listing the learning objectives, which include describing primary and secondary anti-tuberculosis drugs, the phases of TB treatment, mechanisms of action and side effects of drugs, defining multi-drug resistant TB, and the role of vaccines in prevention. It then discusses specifics of TB as a global health problem, treatment regimens, first and second-line drugs, mechanisms of action of isoniazid and rifampin, and side effects of isoniazid. The document aims to educate about best practices for treating TB through use of combination drug therapy.
complete information of tuberculosis including OLD RNTCP and new RNTCP with the novel drug that is marketed; classification of tuberculosis (MDR XDR TDR). special population and tuberculosis treatment clinical presentation and diagnosis
1) TB is caused by Mycobacterium tuberculosis and is one of the top infectious disease killers.
2) It is transmitted through the air and one-third of the world's population is infected with latent TB.
3) Diagnosis involves sputum smear microscopy, culture, tuberculin skin test, chest x-ray and PCR. Treatment requires a minimum of 6 months of multiple antibiotic drugs.
1. Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis that affects the lungs and other organs. It remains a major global health issue, with India accounting for a large number of cases.
2. Treatment involves a combination of antibiotics like isoniazid, rifampin, pyrazinamide, and ethambutol over a period of 6-24 months depending on drug susceptibility and patient category. Directly observed treatment under India's Revised National Tuberculosis Control Programme aims to improve treatment adherence and outcomes.
3. Drug-resistant tuberculosis requires treatment with second-line antibiotics like fluoroquinolones, aminoglycosides, ethionamide, and cycloserine
Mycobacteria are acid-fast rod-shaped bacteria. The most important mycobacteria that cause human disease are Mycobacterium tuberculosis and Mycobacterium leprae, which cause tuberculosis and leprosy, respectively. M. tuberculosis are obligate aerobes that grow slowly over 4-8 weeks on culture medium. They have a cell wall containing waxes and lipids that contribute to their acid-fast staining and ability to evade immune responses. Primary tuberculosis occurs when the bacteria first enter the lungs, while reactivation can occur years later. Diagnosis involves microscopy, culture, or DNA analysis of samples. Treatment requires a multi-drug regimen over several months. M. leprae cannot be cultured but causes
The document discusses Mycobacterium, the genus of bacteria that includes Mycobacterium tuberculosis, which causes tuberculosis. It covers the epidemiology, pathogenesis, diagnosis, and treatment of tuberculosis, noting that it remains a major public health problem, especially in Tanzania where the HIV epidemic has increased the burden of TB. It also discusses other medically important mycobacteria such as Mycobacterium leprae, which causes leprosy.
The document discusses Mycobacterium, the genus of bacteria that includes Mycobacterium tuberculosis which causes tuberculosis. It provides details on the epidemiology of tuberculosis, noting it is one of the top infectious disease burdens globally and in Tanzania specifically. It describes the pathogenesis and clinical presentation of tuberculosis as well as methods for diagnosis and treatment.
Multi Drug Resistance in Tuberculosis Causes and Management Dr Shivansh Verm...shivanshverma55
Multi Drug Resistance in Tuberculosis: Causes and Management
1) Tuberculosis becomes multi-drug resistant when the bacteria develops resistance to both isoniazid and rifampin, the two most effective anti-tuberculosis drugs. 2) Resistance develops through genetic mutations that prevent drugs from binding to their targets in the bacteria. 3) Treatment of multi-drug resistant tuberculosis requires using alternative drugs like fluoroquinolones, cycloserine, para-amino salicylic acid, and injectables that have more adverse effects and toxicity.
This document discusses Mycobacteria and Mycobacterium tuberculosis. It begins by introducing Mycobacteria as acid-fast, aerobic rods. It then discusses the history of discovering M. leprae and M. tuberculosis. Several classifications of Mycobacteria are provided, including M. tuberculosis complex, M. leprae, and non-tuberculous mycobacteria. Extensive details are given on the morphology, pathogenesis, clinical manifestations, diagnosis and treatment of pulmonary and extrapulmonary tuberculosis. Latent tuberculosis and drug-resistant tuberculosis are also summarized.
Mycobacterium are acid-fast, non-motile, non-spore forming bacteria. They include pathogens like M. tuberculosis which causes tuberculosis, M. leprae which causes leprosy, and non-tuberculous mycobacteria (NTM) which can sometimes cause opportunistic infections. M. tuberculosis is transmitted via airborne droplets and causes pulmonary or extrapulmonary infection. Diagnosis involves microscopy, culture, PCR and tuberculin skin testing. Treatment involves a combination of antibiotics over several months. Drug resistant strains like MDR and XDR present a challenge. NTM live in the environment and can cause localized infection, especially in immunocompromised individuals.
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These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
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3. Contents…..
• What is tuberculosis?
• Epidemiological details: Incidence, prevalence, causative agent, host, risk factors
• Pathophysiology of tuberculosis
• Clinical outline: Symptoms & Sign, type to tuberculosis, approach towards
diagnostic confirmation,
• Antitubercular drugs: first line AKT, 2nd line AKT
• Management of tuberculosis: RNTCP program for different types of tuberculosis
• Special consideration: Pediatric Tb, Tb in pregnancy
3
4. What is tuberculosis??
Tuberculosis (TB) is a chronic granulomatous disease caused by mycobacterium
tuberculosis.
It can affect almost any part of the body but primary site is lungs.
As per “WHO” Tuberculosis also called as “ Wasting disease” (pronounced weight loss)
and the “White plague.”
• Neo-latin word : - Round nodule/Swelling
- Condition
“Tubercle”
“Osis”
4
5. TUBERCULOSIS….Epidemiology…..
• TB is the 13th leading cause of death and the second leading infectious killer after COVID-19
(above HIV/AIDS).globally (2018 WHO report)- 2.2 million from India- highest contribution.
• Govt: RNTCP- Revised National Tuberculosis Control Programme: provide free treatment by
government to all TB cases
• On December 30,2019 National Tuberculosis Elimination Program (NTEP) with commitment to
eliminating TB in the country by 2025.
• 2012- NOTIFIABLE disease
• New challenges: HIV- TB infection, MDR TB cases, XDR TB
5
7. 1. Causative Organisms:
it is caused by mycobacterium tuberculosis
Mycobacteriumtuberculosis
Human
Mycobacterium Bovis
Animals
Myco- waxy
appearance- due to
highly lipid
containing cell wall
Bacterium- slender
shape bacillus
7
8. Other causative organisms……..
Mycobacterium africanum
Mycobacterium microti
Non-Mycobacterium Genus
Mycobacterium leprae
Mycobacterium avium
Mycobacterium asiaticum M.
africanum
M. Bovis
M. Canetti
M. microti
M. tuberculosis complex
8
9. 1. Mycobacterium tuberculosis Characteristics…….
Obligate aerobic – grows successfully in oxygen rich tissue like lung,
Non spore forming, Non motile
Facultative intracellular pathogen: usually affect mononuclear
phagocytes( macrophage)
Very slow dividing bacteria – 15-20 hrs
Gram positive rods:
Hydrophobic : Lipid rich cell wall –contain mycolic acid- 50% of
dry weight of cell - Confers many bacterium’s characteristic
- impermeable to dye/stain
- Acid fast- retain acidic stain
- Responsible for resistant to antibiotics
- Resistant to oxidation & survive inside macrophage
- Resistant to lysis by complement system 9
10. • 2. Risk factors
• Immune system can often successfully
fight TBbacteria.
Diseases and medications can weaken
your immune system, including :
• Malnutrition
• Advanced age
• Alcoholism
• Diabetes
• Immunosuppressive medications
• HIV/AIDS & Chemotherapy
• Immigrant (From area with high TB
incidence )
• 3. Transmission & Spread……
• Airborne infection….
• spread by Droplet Infection/
inhalation/ingestion/ placental transfer
10
11. Pathophysiology of tuberculosis…
M.Tuberculosis in inhalation
Enters Host
Lung
Utilizes
Alveoli
Cholesterol in cell membrane (Highly oxygenases amount involved in
metabolism of cholesterol into)
e-
Engulfed by alveolar macrophages and converted into phagosome-
Phagolysosome – M. TB inhibit fusion of Phagosome to lysosome –don’t undergo
degradation
ATP
In lungs- high O2 rich and
oxygenase and best thrive at apex as
have high Oxygen tension.
11
12. Some of Macrophages with I/c MTB express Antigen presenting cell (APC)
APC containing expressed MTB antigen enters lymphatic system and reaches lymphatic
organs.
Activation of TH1cells(Cell mediated Immunity)- Activation of INF-γ on endothelial cells of
blood vessels
Monocyte Adherent Protein (MAP) on endothelium --adherence of monocyte
Squeezing of monocytes from blood to site of injury –converted to Macrophages and increases
in number at alveoli
Granuloma (A group of cluster of epithelioid cells surrounded by rim of lymphocytes
around them Multinucleated giant cells by fusion of adjacent cells (Langhans type)
12
13. 13
1. M.TB entry in lung
2. Inside macrophage
3. Inside lymphatic syste &
Activation of TH1 cells
4. INF on endothelial cell –
MAP – adhesion of monocyte
to endothelium
4a. Squeezing of monocyte
from blood vessels to site of
injury
4b. Monocyte converted into
macrophage – epithelioid cells –
Giant cells
5 Granuloma formation
6 Granuloma located at alveoli
7 Sputum
14. Granuloma consist of macrophage and
Surrounding by the epithelioid cells and giant cells there is a zone of
lymphocytes, plasma cells, and fibroblasts. Hard tubercle: (due to
absence of central necrosis)
Within 10-14 days, the center of the cellular mass undergoes necrosis
CASEATION NECROSIS (soft tubercle)
Wide spread of Soft tubercle over various parts of alveoli and lungs
causes -PULMONARY TB.
Newly formed granulomas damages tissue and degenerates tissue
surrounding
Extensive spread and damage of various parts of body occurs. This
condition is called MILIARY TUBERCULOSIS.
14
15. When infected person coughs or sneezes, the granulomas that may be present
in sputum comes in contact with air.
Lymphocytes, fibroblasts surrounding the cluster of epitheloid cells become inactivated.
And Mycobacterium tuberculi gets free from epitheloid cells
Comes in contact with another person
Through inhalation
New person develops TB
15
17. Type of tuberculosis..
Pulmonary TB Extra pulmonary TB
Less common forms
i. Lymph node TB
ii. Pleural TB
iii. Skeletal- bone TB
iv. Genitourinary TB
v. Miliary TB
vi. Pericardial TB
vii. Gastrointestinal TB
viii.Tuberculous Meningitis
17
21. Specimen
Fresh Sputum
Pleural Fluid
Cerebrospinal Fluid
Urine
Biopsy Material
Gastric Washing
Blood.
21
• 1.Smear test:
a. Zeihl-Neelsen stain
b. Auramine stain(fluorescence microscopy)
• 2. Sputum culture test:
a. Lowenstein –Jensen(LJ) solid medium: 4-
14days
b. Liquid medium : 8-14 days
c. Agar medium : 7 to 14 days
Gold
Standard for
diagnosis
23. Tuberculin skin test (PPD)
Injection of fluid into the skin of the lower arm.
48-72 hours later –checked for a reaction.
Diagnosis is based on the size of the wheal.
1 dose = 0.1 ml contains 0.04µg Tuberculin PPD.
23
28. How to describe any antitubercular drug????
• Action of drug –Bacteriostatic/ Bactericidal
- Extracellularly-E/C (fast multiplying) , Intracellularly –
I/C, (Slow multiplying), Dormant
- Effective against Acidic (active lesion) / alkaline
medium (in Caseous material)
• Mechanism of action:
• Resistant : Incidence, mechanism of resistant
• Pharmacokinetic: tissue distribution, drug drug interaction
• Dose
• Adverse drug reaction
28
29. …So in granuloma, there are
subpopulation need to be affected by
drugs
1. Fast growing- within wall of cavity-
high O2-neutral PH-E/C
2. Slow growing – at inflamed side- I/C –
multiply at low PH (Acidic PH)
3. Spurters- within caseous material – PH
neutral- bacilli grow intermittently -
occasionally active
4. Dormant- inactive for prolonged
period- no drug work on that
Active lesion Neutral PH
Caseous material
I/C – acidic PH
29
31. • Mechanism of resistant:
• 1 in 106 tb bacilli inherently resistant
• Mutation in CATALASE – PEROXIDASE
GENE (Kat G)- most common mechanism-----
stop INH
• Mutation in kasAgene
• Mutation in InHa gene: Over-expression of the
inhA & aphC gene (detoxify organic peroxide)-
Overcome by “High dose INH)
• Global INH resistant- 7.4%, India: 18%
• NO CROSS RESISTANT to other
ANTITUBERCULAR drugs
Mechanism of action
Isoniazide
Catalase peroxidase (enzyme of
mycobacterium) activates
reactive metabolite Adducts with
NAD
InH a Kas a dihydrofolate
reductase
Inhibition of Inhibition of
Mycolic acid DNA synthesis
Bactericidal action
NADP
31
①
②
32. 1. Isoniazid ( Isonicotinic acid hydrazine, H)
• Excellent , Cheapest and essential component of antiTB regimen
• Action on : - Bactericidal
- kill fast multiplying
- inhibit slow multiplying
- E/C, I/C
- Equally effective against acidic/ alkaline media
• Mechanism of action : Mycolic acid synthesis inhibition –unique fatty acid
component of mycobacteria- high selectivity of INH to bacteria
32
33. •P/K
Absorption: Completely absorbed
Distribution: Penetrate all body tissues, tuberculous cavities, meninges, placenta
Metabolism: Liver- N acetylation – Determine ADR but not affect efficacy
• Rate of acetylation depends-
- Slow acetylators (30-40% Indian-(Half life- 3h)- TOXICITY
- Fast acetylators (60-70% Indians- Half life-1h)- THERAPEUTIC FAILURE
- Daily regimen: don’t affect
- But biweekly regimen are less effective in fast acetylator.
- ADR- common in slow acetylator
• DI: H- retard absorption of Phenytoin, CPZ, warfarin, theophylline
33
34. INH: ADR
Dose related ADR
1. Peripheral Neuritis:
Dose related- More with higher dose
Due to interfere with inhibition of pyridoxin utilization
More observed in – diabetics, alcoholics, malnourished, pregnant
& lactating mother
Start prophylaxis – pyridoxin -10mg/ day
Treatment - pyridoxin -100mg/ day
2. Hepatotoxicity : Major dose related ADR:
Common in adults/ alcoholics- abdominal symptoms- go for LFT-
Stop drug- reverse on stopping
Non dose related
Rashes,
anemia,
lethargy,
arthralgia
35
Dose: In adult– 300mg O.D or 5mg/kg/day
35. 2. Rifampin (Rifampicin/ R )
• Semisynthetic derivative of antibiotic- Rifamycin- obtain from bacteria- streptomyces
mediterranei
• Spectrum of Action:
Bactericidal
M. TB: Highly efficacious like INH- affect all subpopulation
E/C, best I/C (slow dividing), (intermittently dividing) Spurters
Good sterilizing & resistant preventing action
M. leprae
Gram+Ve (Staph)
Gram-Ve (E/K/Pse/Pr, legionella, N.Meningtidis H. influenzae)
36
36. • Mechanism of action: Rifampicin
Inhibition of R.N.A
synthesis
Tuberculocidal effect
• Don’t bind to mammalian RNA polymerase
• Resistant: less 10-6 Unusual
• rpoB gene mutation – affinity to drug
• Cross resistant to only congeners not to other AKT
Binds to the β subunit of DNA-dependent RNA polymerase
(rpoB) .
• P/K
• Absorption: food
bioavailability- always
taken in EMPTY
STOMACH
• Widely distributed-
Case/I/c, placenta
• Metabolism : Liver –
EHC
37
37. • Rifampicin: Drug Drug interaction
Microsomal enzyme inducer - Increases level of below enzyme and hasten metabolism-
decrease therapeutic concentration and therapeutic failure result
CYP3A4, CYP2D6, CYP450, CYP1A2, CYP2C
Enhances its own metabolism – other drugs like
- warfarin
- OC Pills (failure of contraception)
- Sulfonylureas (hyperglycemia not controlled)
- Corticosteroid (therapeutic failure)
- HIV Protease inhibitors (NNRTIs)
- Theophylline, Clarithromycin
- Metoprolol
- Antifungal (fluconazole, ketoconazole)
- Phenytoin
Therapeutic failure
Need to increase
dose
38
38. Adverse drug reaction: Rifampicin
FLU like symptoms: Minor-
don’t require drug withdrawal
Hepatitis- Dose related –
With preexisting condition
Stop drug – Reversible
Cutaneous : Flushing, Pruritus
+Rash on face and scalp, redness –
Don’t require withdrawal of drug
Abdominal symptoms:
Don’t require drug withdrawal
39
39. • Dose: 600 mg OR 10 mg/kg OD Oral
Therapeutic uses of rifampicin
• TB: Standard regimen of RNTCP for sensitive TB cases
• Brucellosis – in combination with doxycycline (first choice combination)
• Leprosy – in combination with dapsone
• Prophylaxis of meningitis caused by meningococcus(600mg B.D
for 2 dayz) by H.influenza (600mg/day for 4 days)
• Rifampicin can also be used for prosthetic valve endocarditis.
40
40. 3. PYRAZINAMIDE(Z)-Nicotinamide analogue
Mechanism ofAction
PYRAZINAMIDE
Pyrazinoic acid (POA+)
Inhibit the mycolic acid Synthesize
Pyrazinamidase/Nicotinamidase
41
Enter M.tuberculosis
pncA
M/A : Similar to INH-– Cell wall synthesize
Action : Bactericidal
Highly effective in Acidic PH
Lethal to I/C organism & at inflammatory
site -
Best result is seen when used in initial phase
of therapy- Good sterilizing properties
Shorten duration of treatment & Decrease risk
of relapse : So pyrazinamide is added in first 2
initial months of therapy.
Resistance: mutation of pncA, only if used
alone.
41. • P/K:
• Good CSF distribution – useful for meningeal TB
• Dose: 25-30 mg/kg /day
Safe during pregnancy
• ADR:
• Hepatotoxicity (Dose related, C/I –liver disease)
• Hyperuricemia- gout can occur
• Abdominal distress, arthralgia, fever
• Cautious: DM- repeated blood sugar monitoring done.
42
42. 4. Ethambutol
M/A: Inhibition of mycobacterium cell wall synthesis- but target is different
Aarabinosyl transferase inhibition
Inhibit Arabinosyl transferase-Шenzyme –encoded by gene embA
Disrupt the transport of Arabinosesugar
Arbinogalactan biosynthesis impaired
Disruption in mycobacterial cell wall formation
Interreference of mycolic acid incorporation in to mycobacterial cell wall
43
Resistant:
mutation of embA
gene
43. Ethambutol
• Spectrum: M Tb, MAC
Tuberculostatic drug
Fast multiplying bacteria are more susceptible – added to triple drug
regimen hasten the rate of sputum conversion
44
44. • P/K:
• Metabolism: liver & kidney – Caution for patients have kidney disease
• ADR:
• Patient's acceptability is very good: low S/E
• Visual side effect: Dose/ Duration related side effect
• lose of visual acuity/ colour vision, retrobulbar neuritis leads – tubular vision
• Stop medicine- at first complain of impairing vision
• Children are contraindicated as they are unable to report
• Dose: 1000 mg OR 15mg/ kg OD
Safe in pregnancy
45
48. 2nd line antitubercular drugs(ATD)
Lower efficacy- weaker than 1st line ATD
Higher toxicity (even though good efficacy) –poor patient tolerability
Effective against Resistant organism - “M.TB resistant to first line
antitubercular drug”
Used in RESISTANANT TB : only when first line drug failed
Monitoring of ADR is must while using 2nd line ATD
Expensive
50. Bedaquiline
Grouping of ATD drugs according to hierarchy in efficacy and/ priority in use
Rifabutin,
Rifapentine
51. Description of individual group…
• M/A
• Action on type of mycobacteria (resistant/ atypical mycobacteria/
mycobacterium avium complex-MAC)
• Cross resistant
• Adverse effect profile and its monitoring
• Doses of individual drug
• Specific drug selection in group for “management of Resistant TB”
53. Group 2: Injectable drugs: Kanamycin & Amikacin
• M/A: Inhibit protein synthesis
• Spectrum of Action:
• Sensitive to
S resistant strain
MDR (R+H) strain of M.TB
• Resistant: Cross resistant
• ADR- Equally nephrotoxic but produces less
vetibulotoxicity than hearing loss.
Patient should be warned to report if
tinnitus or vertigo occur
Audiometry and RFT monitoring is must.
RNTCP prefer this drug
Kanamycin (Km)
More toxic but LESS
EXPENSIVE
750mg-1000mg/day
Amikacin(Am)
LESS TOXIC but
More expensive
Other country prefer
this drug
54. Capreomycin (Cm)/ – Alternative to aminoglycoside
• Polypeptide antibiotic- chemically differ from aminoglycoside
• Action: same- Mycobecteriocidal
Effective against Resistant to S / Am respond to Cm.
MDR (R+H)- TB
• ADR: Ototoxicity/ Nephrotoxicity
• parenteral administration- I/M- injection site pain, fever, Rash,
eosinophilia additional side effects.
• Used as ALTERNATIVE to aminoglycoside
HRZE
S
Am
Cm
56. 3. Fluroquinolones FQs (Mfx /Lfx /Ofx /Cfx)
• M/A: Inhibit DNA polymerase
• Action : Mycobactericidal
• FQ is best 2nd line drug because…….…
- Potent,
- Bactericidal,
- Orally active
- Sensitive to MAC, M. fortuitum ,
atypical mycobacterium
- Penetrate cell kill microorganism
inside macrophage as well
Well tolerated 2nd line ATD
GIT- abdominal
pain/nausea/
diarrhea
CNS- headache,
insomnia, dizziness,
Tremor, seizure
Hypersensitivity
reaction: rash,
pruritus,
photosensitivity
ADR -FQ
Q-T prolongation
M
M
57. • Most active is Mfx followed by Lfx – Ofx – Cfx
• Cfx- More active on Atypical mycobacteria
• Mfx: Most active but more CNS, CVS side effects
• Lfx: Good pharmacokinetic profile and less side effect
Lfx: Standardized regimen forMDR –
TB management by RNTCP (2016)
Dose: Mfx- 400mg,
Ofx- 800mg
Lfx- 1000mg
59. 4. Ethionamide(Eto) & 5. Proethinamide (Pto)
• Similar to INH, same mechanism (different gene Eto) but LOWER efficacy
• Action on Atypical mycobacteria and MAC
• Frequent ADR : POOR tolerability
Abdominal discomfort
Hepatitis
Peripheral neuritis- pyridoxin prophylaxis needed
Behavioral changes
Endocrinal disturbance
Goiter
So start with lower dose: 250mg/ day- 750mg/day
RNTCP- standardized regimen for
MDR-TB,
MAC infection in AIDS patients
Reserve drug for leprosy
60. 6. Cycloserine (Cs) & 7. Terizidone
• M/A: It is D-alanine analogue and hence it
replaces alanine which is essential for cell
wall synthesis.
• Bacteriostatic
Action on :
- H/R resistant MTB
- MAC
- Gram+Ve, Chlamydia, E.coli
• ADR : Neurological side effects
❶ ❷
62. 7. Terizidone
Two molecule of cycloserine
Same M/A and same antibacterial properties.
Less neurotoxic
A substitute of Cs especially in genitourinary TB as it attain higher and
sustained concentration into urine.
• Dose- 500-750mg/ day
63. 8. PAS- Paraaminosalicyalic acid
• Chemically similar to Sulfonamide
• M/A- Inhibit folate synthesize of MTB
• Action - Static- least active drug –but delays development of
resistant
• ADR:
• Poor acceptability – because
• ADR- GIT disturbance: anorexia, nausea ,epi pain
• Rashes, fever, malaise, Hypokalaemia , Liver damage, goitre
• Used as sodium salt (Na+ overload) and Ca salt (gastric
intolerance),
64. PAS ; Don’t add to efficacy to more active drug that are given with it
but it delays development of resistant.
MDR-TB Standard regimen only
Dose: 200mg/kg
10-20g/day in divided doses
When other 2nd line cidal drugs
(Km, Ofx, Z, Eto) or both static
(E, Cs) cant used.
65. 9. Rifabutin
• Action: More action on- MAC
• Resistant :Cross resistant to R- MDR-TB
• P/K: Weaker enzyme inducer-
• Use:
Treatment of MAC infection in HIV-AIDS
to avoid drug –drug interaction between
antiretroviral drug ( NNRTI,PI) +
antitubercular drug (R)
Prophylactic: Rifabutin- 300mg/ day or
Azithromycin/ clarithromycin
Treatment : Rifabutin is prescribed with 2-3
antiMAC antitubercular drugs.
Dose & ADR : similar to R
10. Rifapentine
Same M/A, spectrum, Potent enzyme
inducer/ drug- drug interaction /cross
resistant
P/K- longer t1/2 (13-15hr)
Only indication is it can be used in
continuation phase once or twice weekly
as rifampicin substitution of TB treatment
Not suitable for intensive therapy
Latent TB Rx : INH + Rifapentine – once
a week regimen
Rifampicin- Drug sensitive
TB RX
Rifabutin MAC infection in
HIV-TB RX
Rifapentine substitute of R in
continuation phase - Drug sensitive
TB RX
66. 10. Clofazimine
• Dye- Antileprosy drug
• M/A: Interfere with template function of DNA
Alteration of membrane structure
Disruption of mitochondrial electron chain
• Antiinflammatory property
• Spectrum: M. Lepre, resistant M. TB
• ADR: Gi uspet, Skin reaction , discoloration of hair and body secretion
• Avoided during pregnancy
• USE: DR tuberculosis: RR/ MDR TB
68. Bedaquiline (Bdq)
• USFDA approval in 2012 – SIRTURO, 2016 in India
• M/A : BDQ inhibit mycobacterial ATP synthetase – limiting
energy production
• Action: Bactericidal– Very low MIC – for MDR TB and XDR-TB strains : DS, MDR, PreXDR,
XDR strain of mycobacteria, M.Leprae
• Resistant – Mutation of ATP synthetase enzyme and efflux
NO cross resistant to any 1st /2nd line ATD
• P/K- CYP3A4- drug inhibitor/ inducer- drug drug interaction
• ADR: Nausea , headache, arthralgia, QT prolongation, hepatotoxicity.
69. Week 0–2: BDQ 400 mg (4 tablets of 100 mg) daily (7 days per week)
Week 3–24 BDQ 200 mg (2 tablets of 100 mg) 3 times per week (with at least 48 hours
between doses) for a total dose of 600 mg per week
• USFDA approval in 2012 – SIRTURO, India in 2016 -RNTCP introduced BDQ at
selected centres through “conditional access programme”
• Indication/ Recommendation :
Rx of only pulmonary MDR TB adult (>18yrs) when no optimum regimen
constructed.
Use in combination with 3-4 (Sensitive) anti TB drugs for maximum 24week.
Each tablet should be taken with meal.
Must NOT used for DS-TB OR Extrapulmonary TB, nontubercular mycobacterial
Women receiving BDQ should be nonpregnant.
Dose:
70. Pretomaind
• Bicyclic nitroimidazole- Prodrug
• USFDA 2019- highly resistant TB
• M/A: Inhibit cell wall synthesize, depetion of ATP- direct cell
toxicity
• Act on I/C, Persisters
• Resistant: fgd gene- drug activation
• Dose: 200mg OD
• Use: in Resistant TB only
• ADR: GI upset, headache. QT prolongation
• Pregnancy:?????
71
71. Delamanid
• Prodrug- same as pretomanid
• Gene involved: fgd 1 and fbi A
• Safest and most effective drug for MDR TB patients
• ADR: GI Upset, headache, QT prolongation
• Resistant: mutation to fgd1 and fbi A
• Dose: 100mg BD -24week with OBR (Optimized background
regimen)
• Only used with “ Compansate use” after prior approval form DCGI.
72
72. General criteria for using newer drugs ( Bdq, Dlm)
• Patients of MDR- TB/ RR TB > 6years as follows
age >18yrs : Bdq and Dlm can be given
Dlm can be given to children and adolescenc aged 6-17years
Approval from DCGI required for using Bdq and Dlm for age 3-
6years
Nonpregnant female/ postmenopausal/ on non hormonal contraceptive:
can be used for 2 yrs
Patient with stable arrythmia only after cardiac check up
Exclusion: Pregnancy and lactation, arrhythmia
73
74. 1. Aminoglycoside- Km/ Am- Oto/ nephrotoxicity , S Resistant strain/ MDR TB, Km – used
in RNTCP- MDR –TB Mx
2. Cm- : Alternative to aminoglycoside , used when S/Am resistant
3. FQ (Mfx –Lfx- Ofx- Cfx): Best 2nd line oral drug – effective against MDR / Atypical myco/
MAC- well tolerable, Lfx in MDR TB Mx regimen by RNTCP.
4. Eto/ 5. Pto : INH similar – poor tolerable-GIT/PN/CNS/Endo- use : RNTCP-MDR TB
/MAC infection
6. Cs: D alanine analogue – Static -slow resistant development- NO Cross resistant-
Neurological ADR- use : Mx -RNTCP-MDR TB
7. Terizidone: Less neurological ADR- genitourinary TB
8. PAS: similar to Sulfa drug- Static- Poor tolerable (GIT/hypokelemia/goitre/liver damage),
used when resistant to this drugs (4 cidal+ 2 static -Km, Ofx, Z, Eto, E, Cs) or cant be used.
75. 9. Rifabutin: less d-d interaction- replace Rifampin in Rx of MAC infection in HIV
patients
10. Rifapentine-long t1/2- substitute of rifampin –used continuous phase- once or
twice weekly instead of daily regimen.
11. BDQ: Only in selected cases of MDR TB, XDR- QT prolongation, hepatotoxicity
MDR –TB
Km
Lfx
Eto
Cs
MAC
Cp/Lfx
Rifabutin