2. OUT LINE
Introduction
Epidemiology
Microbiology
Pathogenesis
Clinical manifestation
Rx outline
Cx of tbc
3. INTRODUCYION
Mycobacterium tuberculosis
Can affect any organ
Commonest cause death among infectious disease
E-merged 1980s ….AIDS
Current main problem …drug resistance
4. EPIDEMIOLOGY
Affects 1/3rd of world popn
Cmn among HIV infected ,low socioeconomic status
9 mill cases - annually world wide
2 mill deaths annually
>90% of cases /deaths were from developing countries
5. IN ETHIOPIA
100,000 cases occur annually
Death 3000 annually
MDR -TB
180 pt enrolled on Rx
200 on waiting list
6. MICROBIOLOGY OF MTB
Rod shaped , thin , non spore forming , non motile
,aerobic bacterium
Neutral on Gm stain
Once stained cant be decolorized by acid /alcohol
o Classification as AFB
due to CW structures
mycolic acid >60% of cell wall
9. Contd
o After 3 weeks
Two host response will develop
Macrophage activating CMI
Tissue damaging DTH
Balance b/n the 2 –determine the form of Tbc
Granulomatous lesions (tubercles)Formation
In the majority of cases
Cavitiery lesions
10. The bacilli have 4 potential fates:
o may be killed by immune system.
o may multiply and cause primary Tb.
o may become dormant and remain asymptomatic
o may proliferate after a latency period.
11. Clinical Manifestation
Pulmonary Tuberculosis
Classified as primary & post primary [secondary]
Primary Disease
Occur soon after initial infn
Middle & lower lung zones
Usually peripheral
Accompanied >1/2 by hilar & paratracheal LAP
12. contd
Majority of lesion heal spontaneously
Evident by small calcified nodule-Ghon complex
10 tbc progress to clinical illness - In children & Imm
compromised
Initial lesion inc in size & evolve in d/t ways
Pleural effusion [2/3rd]
13. contd
Cavitation
LAP –compress bronchi –obs - segmental/lobar collapse
Partial obs –obstructive emphysema ,& bronchiectasis
may develop
Hematogenous diss [cmn & often asymp]
May result in sever form in imm.comp.
Milliary / meningitis
14. Post primary/Adult
type/Reactivation/Secondary Tbc
From endogenous reactivation
Localized
Apical / post segment of upper lobe
Superior segm. Of lower lobe
Extent varies - from small infiltrates to extensive
cavitary disease
16. Extrapulmonary Tuberculosis
Is seen more commonly in HIV-infected
individuals
all organ systems may be affected
Common site L/N ,Pleura , GUS , Bones & joints
17. Pleural Tuberculosis
accounts for ~ 20% of extrapulmonary cases
Is common in primary tuberculosis
may result from
contiguous spread of parenchymal inflammation
Actual penetration by tubercle bacilli in to the
pleural space
the effusion may be small , and resolve
spontaneously
Or may be sufficiently large
Cx –trapped lung , bacterial contamination
18. Investigations
CXR -effusion & parenchymal lesion
Pleural fluid analysis
Cell count
Biochemical ( PH , glucose , LDH , protein)
Bacteriological ( AFB ,Culture )
Pleural Bx = 80%
Adenosine deaminase (ADA) is a useful screening test:
tuberculosis is virtually excluded if the value is very low
19. Tb of upper airways
Usually a Complication of advanced cavitary PTb
May involve larynx , pharynx and epiglottis
Sym - hoarseness,
dysphonia, and
dysphagia , chronic productive cough
Ulceration - may be seen on laryngoscopy
Ca of larynx - may have similar feature.
Dx - AFB , biopsy
20. HIV-Associated Tuberculosis
Most common disease
Can occur at any stage
High CD4 – typical presentation
Low CD4 – 10 tbc like pattern ,
milliary / diffuse infiltrate ,
little / no cavitation
Overall sputum smear yield is low
Dx is difficult [atypical CXR , sputum low yield]
21. Diagnosis of Tuberculosis
AFB microscopy [sensitivity =40-60%]
a) Light microscopy
• Ziel- Neelson basic fuchsin dyes
• Kinyoun dyes
b) Fluorescence microscopy
• Auromine-rhodomine staining
25. Rx out line
Medical Rx
Drug sensitive Tbc almost all can be Rxd with
standard short course regimen !!!
4 drug regimen [2 mon] [ H , R , Z ,E ]
2 drug regimen [4 mon] [ H , R ]
Surgical Rx
Is indicated only for complication !!!
26. Complication of Tbc
Failure of medical therapy
Progressive disease ,lung destruction ,drug resistance
Massive hemoptysis
Empyema
Bronchiectasis
Fibro thorax
Broncho stenosis
cavernoma
Bronchopleural fistula
Tracheo or bronchoesophageal fistula
Lung cancer
Middle lobe syndrome
27. contd
1. Drug resistance –arise by spontaneous point
mutation
MDR-TB
Resistance for at least H & R
XDR-TB(extensively )
Resistant to at least the fluoroquinolones
and one or more of the injectable drugs
amikacin, kanamycin, or capreomycin
Higher incidence in HIV infected individual
28. contd
Indication for surgery
Same as drug sensitive
Also for -persistence cavietery disease , destroyed
lobe or lung
It should be localized & pt should tolerate surgery
Pre & post op chemotherapy –
Prior medical Rx of 3-6 mon is indicated
Post operatively average - 8mon
29. contd
2 . Hemoptysis
massive >600ml/24hr
causes
Active tbc
Aspergillosis
Bronchiectasis
Lung ca arising from tbc scar
30. contd
a) Active Tbc
Majority-from erosion of bronchial artery which
become abundant around infected site
Also from RASMUSSENS ANEURYSM [when TB extends
into the adventitia and media of bronchial arteries,
resulting in inflammation and thinning of the vessel wall;
this aneurysm subsequently ruptures into the cavity]
Occasionally from small branches of pulm vessels,
acute tuberculouse ulceration of bronchial mucosa
31. contd
b)Aspergillosis
A. fumigatus
Aspergillus is considered an opportunistic pathogen
Requiring : cavieties , asthma / CF , or imm
compromization
The disease has 4 forms
32.
33. contd
Aspergilloma [fungus ball]
Aspergilloma characterized by a mass of fungal
mycelia, inflammatory cells, mucus and tissue
debris, all within a preformed lung cavity
The fungus ball is mobile within the cavity and usually
does not completely fill the space
34. contd
The true incidence of aspergilloma is unknown
Most aspergillomas are asymptomatic
35. contd
Hemoptysis is the most common presenting symptom
Hemoptysis is -due to chronic irritation
When hemoptysis is present, it is generally mild, but it
can be severe and life-threatening
chronic cough and weight loss can also occur
36. Investigations
On CXR:
-revel mass in a preexisting
cavity
- crescent sign, Monad’s sign
On CT:
- provide better definition of mass within
the cavity.
- May demonstrate multiple Asprergillomas.
37. contd
Bronchoscopy - to localize hemoptysis
Serology(Ig E, Ig G) - Most patients have
serum +ve Ab
sputum cultures +ve 50% of the time
38. Treatement
Medical care:
- antifungal agents( Itraconazol)
-not effective
Surgical care:
Indication:
Massive and recurrent hemoptysis
If the lesion is close to main vessel
.
39. 3. Bronchiectasis
Feature
Cylindrical type
Upper lobe (Dry bronchiectasis )
May be asymptomatic or have dry cough , Hemoptysis
4. Empyema
Usually result of ruptured cavieties in to pleural space
BPF - ruptured cavieties in to pleural space
- erosion of empyema in to lung parenchyma
Extensive fibrosis with gross thickened pleura
40. 5. Lung cancer
Linkage –2 d/t ways
1. Tbc can be reactivated by bronchogenic car
Localy by erosion of encapsulated caseous foci
Systematically-debilitation
2. Dvt of malignancy in areas of scar
So both disease can co-exist
Histo Type – undifferentiated carcinoma ,
adenocarcinoma
SCC - More peripherally based Ca will develop
CXR - findings that suggest concomitant Ca :
Progression of one area while the remainder of the lesion is
regressing.
A large >3cm mass lesion admixed with infiltrative disease
41. 6. Middle Lobe Syndrome
Isolated atelectasis of the middle lobe
Also can involve the lingula
Is due to extrinsic nodal compression of the bronchus
which results in post obstructive atelectasis and
chronic pneumonitis
The predominant symptoms are
recurrent infection and
atelectatic middle lobe on chest radiograph, with or
without hilar LAP
42. contd
Bronchoscopy often shows a tight stenosis of the
middle lobe bronchus
it is important to rule out endobronchial obstruction
by a malignant neoplasm
symptomatic patients fit for surgery should undergo
pulmonary resection.
43. 7. FIBROTHORAX
results from fibrosis of the visceral pleura
two mechanisms for formation of fibrothorax
Most often, may develops from pleural inflammation in
patients with pleural effusions
e.g. - incompletely evacuated hemothorax, tbc effusion, or
chronic empyema
Less frequently, results from pulmonary parenchymal
disease
e.g. inadequately treated tbc, bronchiectasis, or lung abscess
44. contd
Any of above process lead to pleural scarring &
dvt of fibrous tissue that replaces & obliterate
pleural cavity.
In severe cases the fibrotic process can invade the
chest wall, destroy the intercostals structures, replace
the endothoracic fascia , cause thickening of
periosteum of ribs, ultimately the ribs can fuse and
calcification of collagen can occur-resulting in a
limitation of resp. excursion and may lead to
development of scoliosis.
The fibrotic process does not traverse the diaphragm.
45. contd
Rx
Best - to make appropriate interventions in patients
with complicated pleural effusions
Decortication – definitive Rx
46. References
Harrison's principles of internal medicine ,17th
ed
Robbins basic pathology 8th ed
Oxford Textbook of Surgery, 2nd ed.
Thoracic surgery 2nd ed[pearson]
Sabiston 7th ed ;cardiothoracic
Schwartzs principle of surgery 9th ed
Up to date 19.1
General Thoracic surgery ,7th ed