"Bronchiectasis: A chronic lung disease marked by irreversible dilation and scarring of the airways."

1. Bronchiectasis

2. Bronchiectasis
Definition
Permanent destructive dilatation of the bronchi (following
infection, destruction and fibrosis)
Types:
Cystic
Cylindrical
Localized or diffuse

3. Etiology of bronchiectasis
 Post-infectious, e.g. tuberculosis, pneumonia; childhood infection
such as measles, mumps, whooping cough
 Connective tissue diseases, e.g. SLE, rheum arthritis, Sjögren’s
syndrome, relapsing polychondritis
Secondary to inhalation or aspiration,
e.g. a foreign body
 Inflammatory bowel disease, e.g. ulcerative colitis
 Allergic bronchopulmonary aspergillosis
 Immune deficiency e.g. Secondary to ch lymphatic leukemia

4. Congenital causes of Bronchiectasis
 Cystic fibrosis
 Ciliary defects, e.g. primary ciliary dyskinesia, Young’s
syndrome
 Kartagener’s syndrome
 Immune deficiency, e.g. IgA deficiency,
X-linked agammaglobulinemia,
Common variable immunodeficiency
 Congenital defects e.g. tracheobronchomegaly (Mounier-Kuhn
syndrome), pulmonary sequestration

5. Clinical Features
 Chronic cough and expectoration
 Sputum: Purulent/ muco-purulent, foul-smelling, large volume, thick and tenacious
 Haemoptysis, sometimes massive
 Recurrent exacerbations
SIGNS: General malnutrition, pallor, edema
Digital clubbing, osteoarthropathy
Chest: Depends on site and extent of involvement
If large, signs of lung volume reduction
May be areas of bronchial breathing
Coarse crepitations, Occasional rhonchi

6. Investigations
 General: Anemia, Hypoglobulinemia
 Chest radiography: CXR, CT scan (HRCT)
 Bronchography
 Sputum examination – For exacerbations.
AFB to exclude TB, if suspected
Smear for culture
ECG, ECHO for cardiac evaluation in suspected
chronic cor-pulmonale

7. Differential Diagnosis
 Pulmonary tuberculosis
 Cystic fibrosis
 COPD
 Allergic broncho-pulmonary aspergillosis
 Interstitial lung diseases
 Eosinophilic lung diseases
 Hypersensitivity pneumonias

8. Radiological features
CXR: May appear normal in early, limited disease,
left lower lobe hidden behind the heart in PA film.
Thickened bronchial lines- tram lines
Cystic shadows/ cavities with fluid levels
HRCT: Almost diagnostic.
Clear demonstration of site of involvement,
Type of lesions, surrounding lung parenchyma,
focal pneumonitis, areas of atelectasis.
Clue to the underlying etiology (eg ABPA)

9. Complications
 Recurrent pneumonias
 Recurrent hemoptysis,
sometimes massive
 Local lung destruction and cavitation
 Aspergilloma formation (fungal ball) in a cavity
 Metastatic spread
 Pulmonary hypertension and
chronic cor pulmonale
 Chronic malnutrition
 Amyloidosis
 Chronic respiratory failure if extensive lung destruction and fibrosi

10. Management
Bronchial hygiene: Postural drainage, Chest physiotherapy
Antibiotics for infections
Expectorant and mucolytics
Management of complications, e.g hemoptyis,
pulmonary hypertension (Chronic cor
pulmonale), respiratory failure
Nutritional supplementation
Surgical management: Resection, if localized
Management of hemoptysis
Lung transplantation ?

11. Recommendation for antibiotics use
Bacterial infection First choice Second line
Haemophilus influenzae Doxycycline,
or Moraxella catarrhalis Co-amoxiclav ciprofloxacin
Streptococcus pneumoniae Amoxicillin Clarithromycin
MRSA Rifampicin and Rifampicin and
trimethoprim doxycycline or
or IV vancomycin linezolid
or teicoplanin
Ps aeruginosa Ciprofloxacin Ceftazidime
and tobramycin
or colistin

12. Prevention of infections
 Preventive vaccinations
 Bronchial hygiene measures:
- Chest physiotherapy
- Nebulization/
steam inhalation
- Respiratory muscle exercises
 Long term antibiotic use - Oral
Nebulized

13. Kartagener’s Syndrome
 Ciliary dyskinesia i.e. abnormal ciliary movements
 Genetic abnormality
 Clinical features: Bronchiectasis
Situs inversus,
dextrocardia
Chronic sinusitis
Infertility

14. Allergic Broncho Pulmonary Aspergillosis
Hypersensitivity to aspergillus in the tracheo-bronchial tree in patients with chronic
asthma.
Clinical Features: Severe attacks, sputum production; hard brown plugs; hemoptysis
Radiology: CXR and HRCT: Fleeting opacities, typical patterns; bronchiectasis –
proximal bronchi
Diagnosis: Skin test: Immediate & delayed +ve
Sputum for aspergillus +ve
Serology +ve; Total & Asperg specific IgE levels
Treatment: Anti-inflammatory drugs (steroids),
Anti-biotics, anti-fungals

16. Cystic Fibrosis
 A common condition in Caucasians –
1 in 2500 live births
 Genetic anomaly: Autosomal recessive mutation on chromosome 7; leads
to protein Cystic Fibrosis Transmembrane Regulator, CFTR) abnormality
 Clinical Features: Multi-organ problem
Bronchiectasis – thick viscid sputum
Pancreatic insufficiency - diarrhoea
Liver disease – biliary cirrhosis
Sweat glands function abnormality
Infertility
Low bone mass

17. Cystic Fibrosis- Diagnosis
Clinical features – Failure to thrive
Intestinal obstruction
Adults: Respiratory infections
Radiological investigations, CXR, HRCT scans etc
Positive sweat Test – High sweat chloride & Na
levels on pilocarpine stimulation
Gene analysis – demonstration of CFTR
mutations

18. Cystic Fibrosis- Treatment
 Treatment of respiratory infection with antibiotics: Anti-
pseudomonas cover
 Reduce sputum viscosity- mucolytics
 Improve airway clearance
 Management of pancreatic insufficiency
 Correction of malnutrition – high calorie, high fat diet;
supplemental vitamins
 Gene therapy
 Lung transplantation

19. TUBERCULOSIS
History
Epidemiology
Introduction

20. What is TB ?
Infection caused by
Mycobacterium tuberculosis (Mtb)
i.e. Tubercle bacillus (T.b.)
Airborne – spreads by aerosols;
enters the lungs through inhalation

21. HISTORY
Ancient disease since BC era
Also known as
 Consumption
 Wasting
 Phthisis
 “Yakshma”
 King’s evil
 Kochs’ disease

22. TB in Antiquity
Clear evidence of spinal TB
Early Dynastic period (c.3400 BC) Egypt :
Destruction and collapse of thoracic vertebrae with psoas abscess in the well preserved
mummy of a member (Nesperehan) of 21st Dynasty priesthood of Amin.
Cave, 1939
Chinese Civilization
Lung fever and Lung cough (Chinese writings – 2698 BC). Symptom of emaciation,
cough, expectoration of blood and pus; cure was difficult; bizarre remedies – dung of
animals & man, the urine of women and infants, the lungs of the hog and the ashes of hair.
Hall, 1936

23. Babylon civilization
Mention of TB 1948 and 1905 BC:
Code of Hammurabi “His wife who is afflicted with the disease he
shall not put away. She shall remain in the house which she has built
and he shall maintain her as long as she lives.”
Indo Aryans
‘A consumptive who is evidently master of himself, who has a good
digestion, is not emaciated and is at the beginning of the disease the
physician can cure’ and ‘the physician who wants great fame cures a
man attacked by consumption’.
Webb, 1936

24. TB in ancient India (Rajyakshma)
 Rig Veda (1500 BC)
 Ayur-Veda (700 BC)
“… a consumptive … at the beginning of disease the
physician can cure …”
 Laws of Manu (1000 BC)
“… sufferers from TB are unclean …”
Webb GB 1936; Brown L 1941; Keers RY 1978

25. Historical landmarks
 Tubercle bacillus (Mycobacterium tuberculosis): Discovered
on March 24, 1882 by Robert Koch (Awarded Nobel Prize in
1905)
 Discovery of X-Ray (Wilhelm Roentgen, 1895)
 Bacillus Calmette Guerin (BCG)
 Chemotherapy: Streptomycin (1944),
P.A.S., Isoniazid (1952)
Ethambutal, Rifampicin
Other new drugs
Regimens and Strategies

27. Koch’s postulates
 The organism should be found in each case of the
disease
 It should not be found in other diseases
 It should be isolated
 It should be cultured
 It should, when inoculated, produce the same disease
 It should be recovered from the inoculated animal

28. Epidemiology
 Incidence vs Prevalence
 Risk factors
 Disease burden
 Morbidity and mortality
 Global health challenge
 Higher incidence in low income countries
 India accounts for about 30% of global cases

30. TB is the leading single infectious cause of
death in South-East Asia
Number of deaths (1000s)
Deaths from infectious
agents in South-East
Asia
0
100
200
300
400
500
600
700
800
Tuberculosis HIV STD Malaria Tropical
Diseases
Measles

31. TB is the leading single infectious cause of
death in India

32. TB is a Leading Killer of Women
48,000
1,01,000
4,93,000
5,38,000
6,05,000
Tropical
Diseases
STD Maternal
Mortality
Malaria TB
Deaths
among
women

33. Tuberculosis
A Global Emergency
 TB kills 5,000 people a day – 2 million each year
 One third of the world’s population is infected with TB
 More than 100,000 children will die needlessly from TB this
year
 Hundreds of thousands of children will become TB orphans
this year
 HIV and MDRTB will make the TB epidemic much more
severe unless urgent action is taken

34. TB Epidemiology in India
 TB infection (Mx +ve) 40%
 Prevalence (sputum +ve) 0.23%
 Mortality 0.04%
 Overall prevalence 0.51%

35. Burden of TB in India
 2 million new patients per year
 Over 450,000 deaths from TB annually
 TB kills more woman than all other causes of maternal mortality
combined
 More than 100,000 women rejected (due to TB)
 More than 300,000 children leave schools to work as a result of
parental TB
 Annual cost of disease – Rs. 12,000 crores
 Annual direct costs – Rs. 30 crores
 Productive work days lost – 100 million per year

36. Risk Factors
1. Immuno-deficiency states
 HIV infections
 Patients with malignancies, leukaemias, lymphomas
 Patients on immuno-suppressant drugs (e.g. steroids)
2. Malnutrition, drug-users, psychiatric disorders
3. Close contacts of patients
 Infants of sputum +ve mothers

37. 4. Poverty; living in crowded, slum areas;
poorly ventilated houses
5. Alcoholism
6. Tobacco smoking
7. Patients with other diseases (comorbidities)
- Diabetes
- Hypothyroidism
- Silicosis (silico-tuberculosis)
8. Post-operative – gastrectomy

38. HIV Infection & TB Risk
 Annual risk – about 10%
 Life time risk of TB w.r.t. HIV
- Negative 5-10%
- Positive 50%
COINFECTION (HIV & TB)
App. 1/3 of 20 million HIV pts.

39. TB and AIDS
10%
60%
0%
10%
20%
30%
40%
50%
60%
70%
PPD+/HIV-negative PPD+/HIV+
Lifetime Risk
of TB

40. Homeostasis – unbalanced in infections
Host defenses
Pathogens

41. TB – An Infection
 Tubercle bacillus (T.b)
Mycobacterium tuberculosis (MTB)
 Airborne – spreads by aerosols; enters the lungs through
inhalation
 Interplay between the bacillus and the host defences
 Establishment of infection – Lesions in the lungs / lymph nodes
/ GIT/ other organs
 Spread to other sites/ organs
 Complications and Sequelae

42. Sequence of TB infection
1. Inhalation of Mtb – localization in tracheo-bronchial
tree
2. Recruitment of macrophages and lymphocytes.
Macrophages transform as Langhan’s cells
3. Engulfed by alveolar macrophages (defence cells) –
either get killed or destroy the cells to penetrate
alveolar walls and enter the lymphatics/ blood
vessels, reach regional LN

43.  Langhan’s cells and lymphocytes form granulomas
(Primary lesion)
 Primary lesion and regional lymphatics and LN
together called Primary Complex (of Ranke)
 Fibrous capsule formation; may lie dormant in the LN
(Latent TB) or spread through lymphatics/ blood
stream to bones, liver, spleen, GIT etc.
 Impart delayed type, cell-mediated immunity
(demonstrated by Tuberculin or Mantoux test)

44. Bacillary multiplication
1 Bacillus
20 hrs
2 bacilli
10 days
5000 (Nodule)
1 month
> 1 billion (large cavity)

45. Natural history of untreated Primary TB
Time from Infection TB involvement
3-8 wks Primary complex
3-6 mths Meningeal, miliary,pleural
Up to 3 yrs GIT, Bones & joints, LNs
About 8 yrs Renal tract
3 yrs onwards Post primary disease

46. Continuing Infection
One Sputum positive
(untreated, undetected)
Infects
6-12 persons in 1st year
 upto 24 in 2 year life span

47. The National Problem
1. Large pool of patients
2. Renewed and perpetuated
3. Difficult to approach
4. Difficult to find, hold and treat
5. Shortage of beds

48. THANK YOU