TB seminar

TUBERCULOSIS AND mdr tuberculosis. : 

TUBERCULOSIS AND mdr tuberculosis. AMOL GAIKWAD

Tuberculosis : 

Tuberculosis Ancient disease At least 4000 years

What is Tuberculosis ? : 

What is Tuberculosis ? TUBERCULOSIs is a choric granulomatous infection caused by M. tuberculosis complex. Complex consists of :- M.tuberculosis, M.bovis, M.caprae, M.africanum, M.microti, M.pinnipedii M.canettii. It primarily affects Lungs, Intestine, Meninges, Bones, Joints, Lymph glands, Skin,& other tissue of the body. Disease also affects animals like cattle- Bovine TB

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Robert Koch The discovery of the TB germ in 1882 THEN Proof of airborne spread Special staining methods Culture BCG-vaccine injection PPD test Anti-TB drugs developed

Problem statementWorld : 

Problem statementWorld TB is an ancient disease which remains a world wide problem. The importance of TB is evident in the following facts: about 1 in 3 of the world’s population are infected with tubercle bacilli and someone is newly infected every second although most infected people remain asymptomatic, TB causes illness in about 8 million people every year about 2 million people die from TB every year - more deaths than for any other infectious disease CAPTON OF INFECTIOUS DEATHS

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About 95% of the world’s cases of TB occur in the developing countries of South East Asia, Sub-Saharan Africa and the Western Pacific. The largest number of cases occur in South East Asia and this region accounts for 33% of incident cases globally. The highest mortality from TB also occurs in this region. It is estimated that 1-2% of the Indian population are infected with tubercle bacilli. The global incidence of TB has increased in the last two decades. This has been attributed to a number of factors, including: the HIV pandemic emergence of drug-resistant strains of M. tuberculosis poor national TB control programmes and worsening socio-economic conditions in many countries

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9.2 million new cases in 2006 Out of that 4.1 million were smear +ve; of these 7.7% (7,89,000) were co infected with HIV A total of 31.8 million new & relapse cases & 15.5 million new smear +ve cases were notified by DOTS. Programs world wide in 12 year betn 1995-2006 India , China, Indonesia, South Africa & Nigeria rank 1st to 5th in terms of incidence.

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Latest global TB Estimates - 2006 Estimated number of cases Estimated number of deaths 1.65 million (25 per 100,000) 9.15 million (139 per 100,000) ~130,000 489,000 All forms of TB Greatest number of cases in Asia; greatest rates per capita in Africa Multidrug-resistant TB (MDR-TB) Extensively drug-resistant TB (XDR-TB) ~35,000 ~20,000 HIV-associated TB 709,000 (8%) 231,000

Estimated TB incidence rate, 2006 : 

Estimated TB incidence rate, 2006 No estimate 0–24 50–99 100–299 300 or more 25–49 Estimated new TB cases (all forms) per 100 000 population The boundaries and names shown and the designations used on this map do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement.  WHO 2006. All rights reserved

In INDIA : 

In INDIA Highest TB burden country in world. Account nearly 1/5th (20%) of global burden of TB & 2/3rd of cases in SEAR. Every year approx. 1.8 million person develop TB of which 0.8 million are new smear +ve. 75 new smear positive PTB cases/1,00,000population per year Almost 0.37 million people die every year Over 1000 deaths a day 2 deaths every 3 minutes

India is the highest TB burden country globally accounting for one fifth of the global incidence : 

India is the highest TB burden country globally accounting for one fifth of the global incidence Source: WHO Geneva; WHO Report 2006: Global Tuberculosis Control; Surveillance, Planning and Financing

Estimated Incidence of TB in India*(No. of NSP Cases per 100,000 population, per year) : 

Estimated Incidence of TB in India*(No. of NSP Cases per 100,000 population, per year) North West East South * Estimated from recent ARTI survey ** For programme monitoring purpose estimated cases in East & South zones have been kept at the national level of 75 and this is within the upper limit of CI or ARTI in these zones Source: Module 9, Managing the RNTCP in your area

Age distribution : 

Age distribution

Tuberculosis estimates for India (2006) : 

Tuberculosis estimates for India (2006)

Natural history of TBAgent factor : 

Natural history of TBAgent factor Agent :- M. tuberculosis - intracellular organism M.bovis in cattle In recent years atypical mycobacteria have been isolated Photochromogens – eg. M. kansasii Scotochromogens – eg. M. scrofulaceum Non photochromogen – eg. M. intercellulare Rapid growers. – eg. M. fortuitum

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Source of infection 1.Human & 2. Bovine Human source : A case of sputum +ve for TB bacilli An estimated annual avg. of 10-15 persons contract the infection from one case of infectious PTB Bovine source : usually infected Milk Source factors :- Cavitary lesion Sputum positivity

Host factors : 

Host factors Age :- all age groups Sex :- males Hereditary :- not a hereditary disease but people with DR2 gene leukocytes prone to TB. Nutrition :- Immunity :- immunocompromised due to any reason. No inherited immunity but Nramp-1 (natural resistance – associated macrophage protein 1) which maps to chromosome 2 in human may play a determining role in susceptibility to TB.

Environmental factors : 

Environmental factors Duration of contact with the case Concentration of droplet nuclei in air. Amount of outside air ventilated into the room.

Predisposing factors : 

Predisposing factors Direct factors :- DM HIV infection Silicosis Close contact Incompletely treated open case of TB Immunosuppressive therapy Indirect factor :- Malnutrition Smoking Alcohol Distant factors :- Lack of political commitment Poverty Overcrowding Illiteracy Lack of community awareness

Transmission : 

Transmission Pulmonary tuberculosis is a disease of respiratory transmission, Patients with the active disease (bacilli) expel them into the air by: coughing, sneezing, shouting, or any other way that will expel bacilli into the air

Transmission 1 : 

Nearly all TB infection is acquired by inhalation of respiratory droplets from an infectious contact. Air droplets 3-5 μm diameter coughed, sneezed or spat out by an “open” case of TB. The droplets are inhaled by a close contact. This may lead to a lung infection which then may go on to develop into disease – in the lungs and/or in other organs. NB. Abdominal TB can also result from drinking unpasteurised cow’s milk infected with M. bovis. Transmission 1 How is TB transmitted?

Pathogenesis 1 : 

Between 70-90% of individuals exposed to TB will not develop any symptoms or signs of infection. The reasons for this are unclear but, in view of the known risk factors for infection, they may include inhalation of an insufficient number of organisms to cause infection or adequate immunity to prevent an infection becoming established. Pathogenesis 1 What happens following inhalation of M. tuberculosis?Outcome 1: No infection

Pathogenesis 2 : 

Pathogenesis 2 Following inhalation, TB bacilli settle in the alveoli. This results in a small focus of local inflammation in the lung parenchyma. This primary focus usually occurs in the upper lobes in adults but may occur in any of the lung lobes in children. More than one focus may occur in the same patient. The organisms then spread via the local lymphatics to the nearest hilar lymph nodes, which may then enlarge. The primary focus and the enlarged regional lymph nodes form the primary complex or “Ghon’s complex”. What happens next depends on the size of the infecting dose and the resistance of the host. Most commonly, the primary focus is “walled-off” by the immune system and lies dormant for years. The infection may be reactivated years later if the immune system of the host becomes weakened. Primary focus successfully contained by the host immune system The infected person does not have TB disease and cannot spread TB. However, an immune response to M. tuberculosis will have developed – and can be demonstrated by a positive Mantoux test (see later). What happens following inhalation of M. tuberculosis?Outcome 2: Infection with formation of a primary complex

Pathogenesis 3 : 

Infection not successfully contained by the immune system. Person develops lung disease and becomes an open case - capable of infecting others via respiratory droplets. Pathogenesis 3 The primary focus is not contained and lung disease may develop in several ways: The primary focus enlarges and undergoes central necrosis to form a cavity The infection can spread locally and result in tuberculous bronchopneumonia Marked swelling of the mediastinal lymph nodes may compress large bronchi and result in lobar collapse The enlarged lymph node may act like a one-way valve causing hyperinflation of a lung or lobe Pleural infiltration may result in a pleural effusion which is rich in lymphocytes – a useful pointer to the diagnosis when pleural fluid is aspirated and analysed What happens following inhalation of M. tuberculosis?Outcome 3: Pulmonary disease

Pathogenesis 4 : 

Pathogenesis 4 Haematogenous dissemination of M. tuberculosis leads to granuloma formation in many organs. Examples include: Diffuse infection of the lungs: “miliary” TB Brain: TB brain abscess Meninges: TB meningitis Bones: TB osteomyelitis – commonly affects the spine and is then called “Potts’ disease” Pericardium; TB pericarditis and pericardial effusion Disseminated disease is most likely to occur in the immunocompromised patient (e.g. HIV/AIDS, malnutrition) and at extremes of age. What happens following inhalation of M. tuberculosis?Outcome 4: Systemic disease

Pathogenesis 5 : 

Summary (1): natural history following TB exposure Pathogenesis 5 What are the likely outcomes following exposure to open TB?

Symptoms of Pulmonary TB include: : 

Symptoms of Pulmonary TB include: Cough (usually productive and maybe bloody) Low-grade fever Sweating Chills at night Fatigue Malaise Anorexia Weight loss Dull, aching chest pain or tightness Symptoms of extrapulmonary TB depend on the organ system involved but may include systemic symptoms such as malaise

Clinical features 2 : 

Clinical features 2 Organ specific - examples include: Lungs Cough – usually chronic, Productive of whitish or mucoid sputum in adults but usually unproductive in children Haemoptysis Central Nervous System – may present as TB meningitis Tuberculoma, with the classical features of a space-occupying lesion simulating a brain tumour The lung is the predominant organ affected, being involved in over 75% of cases. General symptoms: Loss of weight in adults or growth faltering in children Night sweats Malaise Anorexia What are the symptoms and signs of TB? 2. Active infection: symptoms

Clinical features 3 : 

Clinical features 3 TB lymphadenitis presents as painless enlargement of the superficial lymph nodes. The neck is the commonest site involving the cervical, submandibular, pre and post- auricular lymph nodes. The lymph nodes are non-tender, matted together and rubbery in consistency. It is common for enlarged lymph nodes to ulcerate and discharge. What are the symptoms and signs of TB? 2. Active infection: signs

Clinical features 3 : 

Clinical features 3 Abdominal TB Pathology affects the mesenteric and the retroperitoneal LN, the omentum and the gastrointestinal tract. Patients may present with weight loss, diarrhoea or constipation, abdominal distension (from ascites) or chronic intestinal obstruction. Enlarged mesenteric lymph nodes may be palpable as multiple intra-abdominal masses. What are the symptoms and signs of TB? 3. Pulmonary and abdominal TB

Tuberculosis of the spine – “Pott’s disease” : 

Tuberculosis of the spine – “Pott’s disease” TB commonly affects the spine, especially in young children, and usually presents as a swelling on the back. The lower thoracic and the upper lumbar vertebrae are the usual sites, however any vertebra can be affected. The patient may also present with kyphosis, scoliosis, kyphoscoliosis, or features of spastic paraparesis. There may be a sharp angulation of the spine caused by collapse of a vertebra – referred to as a “gibbus” A young child from West Africa. Note the swelling over the lower thoracic vertebrae.

Diagnosis of Active TB : 

Diagnosis of Active TB Acid fast stain of sputum Sputum AFB culture (culture needed for drug susceptibility) Radiographic imaging (CXR) Fluid Aspiration Tissue biopsy

SPUTUM EXAMINATION. : 

SPUTUM EXAMINATION. Two samples a) spot b) early morning Smear positive pt Smear negative pt

CXR Findings : 

CXR Findings Primary TB: Lower or middle lobe infiltrates Reactivated TB: Apical infiltrates/cavitation Latent TB: Usually normal Nodules in hilar area or upper lobes Pleural scarring/thickening

Investigation 7 : 

Investigation 7 Other investigations are indicated depending on the organs/ systems affected by the disease Spinal radiographs in Pott’s disease Lymph node aspirate (microscopy, culture and cytology) or biopsy (histology and culture) in TB lymphadenitis Lumbar puncture for cerebrospinal fluid analysis in TB meningitis (microscopy, biochemical analysis and culture) Diagnosis: Other investigations

Newer diagnostic tools : 

Newer diagnostic tools BACTEC ELISA PCR Genotyping by RFLP (Restriction fragment length polymorphism) FTB (fast plaque TB) BAMT (Blood analysis for M.tuberculosis) QTB-G (Quanti FERON TB – Gold)

BACTEC : 

BACTEC Is a rapid culture method Can detect mycobacteria as early as within 7-10 days. Principle :- measurement of production of CO2that is liberated from the metabolism of the organism. The liberated CO2 is measured by radioactive means; and by non radioactive means Radioactive means – BACTEC 460 Non radioactive means – BACTEC 960 But is expensive.

ELISA : 

ELISA Serological test to detect specific antibody response in TB. Patients by using specific antigen (usually A 60 antigen) The antigen is neither specific nor sensitive. So it has only a supportive value mainly in the diagnosis of extra pulmonary disease.

PCR : 

PCR Amplification of target nucleic acid enzymatically by PCR Then using nucleic acid probes for specific detection and identification The test may detect positive signals from 1-10 bacilli in specimen tested in a day. Test requires high level of standardization. Other NAA (Nucleic acid amplification) technique. MTD – (M.tuberculosis direct test) Amplicor TB.

FTB (Fast plaque TB) : 

FTB (Fast plaque TB) Is a site specific and can be performed on sputum, aspirates, pus, blood etc. Can detect viable bacilli, indicating active infection Results are comparable with culture and obtained within 48-72 hrs. Sensitivity is 90% & specificity is 100%

Genotyping by RFLP : 

Genotyping by RFLP Combines southern blotting with hybridization with specific DNA probe to produce characteristic band pattern ( DNA finger printing) The insertion sequence used for TB. Is IS6110 Is can be used to enhance the epidemiological research.

Blood analysis for M.tuberculosis.(BAMT)QFT-G (Quanti FERON TB – Gold) : 

Blood analysis for M.tuberculosis.(BAMT)QFT-G (Quanti FERON TB – Gold) It measures the concentration of Interferon –γ released from blood monocytes after exposure to an antigen specific for MTB. Not expressed by either NTM or BCG vaccine organism. Advantages Decrease false positive rates. no booster effect. result’s only after one visit. Limitations Blood should be processed within 12 hrs. high cost.

Investigation 5 : 

Investigation 5 Mantoux test This test detects a delayed hypersensitivity, cutaneous reaction to a purified protein derivative (PPD) of M. tuberculosis – also called “tuberculoprotein”: Strain used is PPD-RT-23 with Tween 80 PPD is injected intradermally the reaction is read at 48-72 hours erythema and induration at the injection site signifies previous exposure to mycobacteria Not diagnostic Only means of estimating prevalence of disease in the population.

Skin Test Interpretation : 

Skin Test Interpretation Induration ≤ 5 mm – negative. Induration 6-9 mm – doubtful. Induration ≥ 10 mm – positive.

Skin Test Intrepretation : 

Skin Test Intrepretation False positives: Non-tuberculous mycobacterial infection BCG vaccination False negatives: HIV Malnutrition Steroid therapy

Treatment : 

Treatment Before 1940s: open air (sanatorium) 1946: streptomycin 1952: isoniazid 1970: rifampin

Bactericidal & Sterilising drug actions : 

Bactericidal & Sterilising drug actions Time M Tb Rapidly multiplying Slowly multiplying Dormant Isoniazid, Strptomycin Rifampicin (Bactericidal) Rifampicin, Isoniazid Pyrazinamide (Sterilising)

Monitoring on Treatment : 

Monitoring on Treatment INH: Side effects GI irritation Liver damage Blood dyscrasias Rash Paresthesias/weakness – peripheral neuropathy is less likely with pyridoxine Anorexia/fatigue

Monitoring on Treatment : 

Monitoring on Treatment Rifampin: Side effects GI upset Hepatitis Flu-like syndrome – if taken irregularly Multiple drug interactions Orange bodily secretions due to excretion

Monitoring on Treatment : 

Monitoring on Treatment PZA: Side effects GI upset Hepatitis Hyperuricemia – acute gout uncommon Ethambutol: Optic neuritis: reversible decreased red-green color perception and visual acuity Not hepatotoxic

Monitoring on Treatment : 

Monitoring on Treatment Streptomycin: Vestibular damage & nystagmus Renal damage

Classical (Long-course) Chemotherapy. : 

Classical (Long-course) Chemotherapy. It depends on INH along with 1 or 2 bacteriostatic or companion drugs. 18 months of treatment was required. Problems with it are - Long duration. Noncompliance. Drug resistance.

Short-course Chemotherapy : 

Short-course Chemotherapy In 1972, Wallace Fox & his colleagues showed that the addition of Rifampicin or of Pyrazinamide to regimen containing INH made it possible to reduce the duration of treatment. ADVANTAGES Rapid bacteriological conversion Lower failure rates Reduction in frequency of emergence of drug resistant bacilli Good patients compliance Patients become non-infectious earlier DISADVANTAGES High cost of short term chemotherapy

Short-course Chemotherapy DOTS(directly observed treatment) Strategy : 

Short-course Chemotherapy DOTS(directly observed treatment) Strategy It ensure cure by providing the most effective medicine & confirming that it is taken. During the intensive phase patient has to swallow the drug in presence of trained person or a health worker During continuation phase, the patient is issued medicine for a week in multiblister combipack, consumption of medicine is checked by return of empty multiblister combipack.

Anti-TB drugs in multiblister combipack : 

NTF Presentations for RNTCP Sensitization First edition 10th Nov 06 Anti-TB drugs in multiblister combipack Blister packed drugs packaged for IP & CP Category 1 drug box Quality assured drugs packed in patient-wise boxes Category 1 drug box Including for Paediatric Age Group

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NTF Presentations for RNTCP Sensitization First edition 10th Nov 06 Direct Observation of Treatment (DOT)

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Categorisation

Treatment Regimens : 

Treatment Regimens

Follow up sputum examinations : 

Follow up sputum examinations

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Category IV MDR TB cases

Tuberculosis : 

Tuberculosis Active: Positive skin test or Quantiferon test Symptoms Signs Abnormal CXR Latent: Positive skin test or Quantiferon test No symptoms No signs Normal CXR Exceptions: Nodules, pleural scarring

Latent TB : 

Latent TB Life time risk of reactivation of TB among person with a positive TST. Person with HIV infection of evidence of old healed TB on chest X-ray were the highest risk population. Suspects of Latent TB. HIV patients whose HIV status is not known Iv drug abuser Close contact of a newly diagnosed TB patients Person with old fibrotic lesion on X-ray, consistent with prior pulmonary TB.

Treatment of Latent TB : 

Treatment of Latent TB Need to exclude active disease before treatment (avoids single drug therapy of active TB) CXR: if changes consistent with TB, send AFB sputum culture Single drug therapy appropriate for latent TB bacterial load much lower compared with active TB Efficacy of 90% if all the medications are taken 60-70% rates when the drugs are self-administered Protective effect will last probably for life but at least 20 years

Treatment of Latent TB : 

Treatment of Latent TB Regimens: Isoniazid (INH) daily or twice weekly under directly observed therapy (esp. if adherence is an issue) 9 months of treatment is optimal At least 6 months is needed 12 months if treatment is interrupted Rifampin daily 4 months of treatment Alternative regimen for those exposed to an INH resistant patient

Treatment of Latent TB : 

Treatment of Latent TB Regimens: Rifampin/PZA for 2 months Similar in safety and efficacy to 12 month regimen of INH No longer recommended due to hepatic toxicity (including liver failure leading to death)

Treatment of Latent TB : 

Treatment of Latent TB If INH treatment is interrupted, an additional 3 months should be given If interruption is >3 months, re-start treatment If a treated person is re-exposed to someone with TB, repeat treatment is not needed unless the patient is HIV+

Drug resistant Tuberculosis : 

Drug resistant Tuberculosis Causes Incorrect prescription Irregular supply of drugs Non-compliance of treatment Lack of supervision and follow up

Types of resistance : 

Types of resistance Primary or pre-treatment resistance: pt. has not received the drug before Secondary or acquired resistance: bacilli were sensitive to drug at start of treatment but becomes resistant during the course of treatment. Mono drug resistance Poly drug resistance

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The probability of spontaneous resistance is estimated at 10-6 for Isoniazid. The probability of spontaneous resistance is estimated at 10-8 for Rifampicin. Genetic data have shown that at least 2 mechanisms account for INH resistance: 1. Deletion of katG, the gene encoding for catalase 2.Mutatrion in inhA, a gene involved in the synthesis of mycolic acid. Rifampicin resistance result from mutation within the rp0B gene which encodes for β subunit of RNA polymerase.

Treatment of Drug Resistant Active TB : 

Treatment of Drug Resistant Active TB INH resistant TB: Rifampin, PZA, and ethambutol for 6 months Rifampin resistant TB: INH, PZA, and streptomycin for 9 months or INH and ethambutol for 18 months

Drug Resistance : 

Drug Resistance MDR (Multiple Drug Resistance) INH AND Rifampin XDR ( Extreme Drug Resistance) INH and Rifampin plus any floroquinolone and at least one of the three injectable second-line drugs (amikacin, kanamycin or capremycin)

Global Drug-Resistant TB: How Bad Is It? : 

Global Drug-Resistant TB: How Bad Is It? 2004 MDR TB estimates: 424,203 (4.3%)(estimate includes new and previously treated cases) 2000 MDR TB estimates: 272,906 (1.1%)(estimate includes new cases only) Estimated 43% of global MDR TB cases have had prior treatment China, India, and Russian Federation account for 62% of the MDR burden Prevalence of XDR TB not known Zignol, Dye et al, JID 2006:194

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MDR-TB among new cases 1994-2007

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MDR-TB among retreatment cases 1994-2007

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Weighted mean of %MDR TB among new and previously treated cases by region, 2007

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An accurate picture of drug resistance is not available coz only few countries have a reliable drug resistance surveillance system In INDIA MDR – TB in new cases – 3% In retreatment cases – 12-17& Is difficult to treat even though second line drugs are available. Treatment of MDR is more than 2 yrs & still outcome is poor.

MDR TB management : 

MDR TB management Cat II patient who remains sputum positive even 4 months of supervised treatment will be identified as MDR – TB suspect & referred to diagnosis by culture & DTS done at RNTCP accredited IRL. It is categorized as cat IV Regimen – [6(9) Km Ofx Eto Cs Z E] & [18 Ofx Eto Cs E] Total duration- 24-27 months Smear examination monthly during IP & Atleast quarterly during CP; culture should be done at least at 4,6,12,18 & 24 months of treatment.

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BS

Newer anti TB drugsIIIrd line drugs : 

Newer anti TB drugsIIIrd line drugs Rifamycin Oxazolidinone (Linezolid) Nitroimidazopyrans Diarylquinolines It is not prove that how many of these are useful Linezolid :- Inhibit protein synthesis to the 70s ribosomal initiation complex. Active against susceptible / resistant M.TB S/E – Bone marrow suppression dose dependant& reversible Peripheral nuropathy

DOTS – Plus : 

DOTS – Plus Dots – plus for MDR-TB is a comprehensive management initiative built upon 5 elements of dots strategy Goal of it is to prevent further development & spread of MDR-TB The aim of implementation of DOTS-plus in selected areas with significant level of MDR TB is to combact an emerging epidemic.

5 elements of DOTS-plus : 

5 elements of DOTS-plus Sustained government commitment Accurate, timely diagnosis through quality assured culture & drug susceptibility testing. Appropriate treatment utilizing second line drugs under strict supervision. Uninterrupted supply of quality assured anti – TB drugs. Standard recording and reporting system.

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XDR-TB – Extensive Drug Resistance The new threat – 24 March 2006 XDR = Resistance to at least INH and RIF (MDR) PLUS resistance to any fluoroquinolones, AND any one of the second-line injectable drugs (amikacin, kanamycin, capreomycin) Of 17,690 isolates from 49 countries during 2000-2004 20% were MDR and 2% were XDR XDR found in: USA: 4% of MDR Latvia: 19% of MDR S Korea: 15% of MDR XDR found in Southern Africa associated with HIV

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Czech Rep. The boundaries and names shown and the designations used on this map do not imply the expression of any opinion whatsoever on the part of the WHO concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement.  WHO 2005. All rights reserved Ecuador Georgia Argentina Bangladesh Germany Rep of Korea Armenia Russian Fed. South Africa Portugal Latvia Mexico Peru USA Brazil UK Sweden Thailand Chile Based on information provided to WHO Stop TB Department - June 2008 Spain China, Hong Kong SAR France Japan Norway Canada Italy Netherlands Estonia Lithuania Ireland Romania Israel Azerbaijan Poland Slovenia India Australia Mozambique Vietnam Countries with XDR-TB confirmed cases as of June 2008 Ukraine Moldova Philippines Botswana Nepal Islamic Rep. of Iran Lesotho Swaziland Namibia

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The boundaries and names shown and the designations used on this map do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement.  WHO 2006. All rights reserved * Sub-national averages applied to Russia < 3% or less than 3 cases in one year of surveillance 3 - 10% > 10% No data Report of at least one case % XDR-TB among MDR, 2007

XDR : 

XDR The magnitude of problem remains to be determined due to the absence of laboratories capable of conducting quality assured second line drug susceptibility test The prevalence of it is 9% 0f MDR cases. It is much more difficult to treat.

The STOP TB Strategy : 

The STOP TB Strategy In 2006, WHO launched the new stop TB strategy. Core of the strategy is DOTS The strategy is to be implemented over the next 10 yrs i.e. from 2006-2-15 It focuses on the 5 principal indicators that are used to measure the implementation & impact of TB. Case detection Treatment success Incidence, prevalence and death.

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The STOP TB Strategy – version 2008 - draft Pursue high-quality DOTS expansion and enhancement Political commitment with increased and sustained financing Early case detection through quality assured bacteriology Standardised treatment, with supervision and patient support An effective drug supply and management system Monitoring & evaluation system, and impact measurement Address TB-HIV, MDR-TB and other challenges TB/HIV collaborative activities Prevention and control of multidrug-resistant TB Addressing contacts, prisoners, refugees and other highly vulnerable groups and special situations 3. Contribute to health system strengthening Active participation in efforts to improve system-wide policy, human resources, financing, management, service delivery, and information systems Sharing of innovations that strengthen systems, including the Practical Approach to Lung Health (PAL) and infection control in congregate settings Adaptation of innovations from other fields

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4. Engage all care providers Public-public, and public-private mix (PPM) approaches, including NGOs, FBOs and professional societies International Standards for TB Care 5. Empower people with TB, and communities Advocacy, communication and social mobilization Community participation in TB Care Patients' Charter for Tuberculosis Care 6. Enable and promote research Programme-based operational research and introduction of new tools into practice Research to develop new diagnostics, drugs and vaccines

Slide 98: 

Thank you