Pulmonary Tuberculosis

Caused by Mycobacterium tuberculosis

hominis.

The lung is the commonest site.

However, other tissues and organs can be

affected.
 It is estimated that 1/3 of the worlds
population is infected with TB.

However, disease is seen only in 10% of the

cases of infection.

This occurs when the host defenses are

reduced.
 Predisposing factors:
Chronic alcoholism
Diabetes
Immunosuppression (HIV/AIDS)
 TB is a major cause of death in developing
countries.

TB is the principal cause of HIV related deaths

in Africa & the Far East.
Transmission

Usually direct transmission by inhalation of

airborne organisms from aerosols of infected
persons.

Oropharyngeal and intestinal tuberculosis is

contracted by drinking milk contaminated
with Mycobacterium bovis.
CD4+ T cells are important in the cell-mediated
immunity against Mycobacteria.
 The previously unexposed immuno competent
individual develops a targeted cell-mediated
immunity.

This confers resistance to the organism.

It also results in development of tissue

hypersensitivity to tubercular antigens.
 The pathologic features of tuberculosis,

i.e. caseating granulomas

cavitation

are due to the host immune response.

 Primary Tuberculosis
Secondary Tuberculosis
Primary Tuberculosis

Occurs in previously unexposed, un sensitized

individuals.

Lungs are the initial site of contact.

The primary infection is usually asymptomatic.

Is usually a small mid zone, sub pleural, lung

lesion with similar lesions in the hilar nodes.
 Primary Lung Lesion = Ghon focus

Primary lung lesion + lesions in Hilar nodes =

Ghon Complex
Ghon Complex- Grey/white parenchymal lesion with
caseous nodes
Histology - Granuloma

Usually about 10mm diameter

Centre caseous necrosis
Periphery epithelioid histiocytes, scattered
Langhans giant cells &
lymphocytes
Typical Granuloma with central caseous necrosis,
surrounding epitheliod histiocytes, Langhans giant cells and
lymphocytes
Sequelae

Almost all lesions heal leaving a fibro

calcified nodule in the lung
no clinical sequelae
In some - latent lesions
viable bacilli may persist within
these foci

Nidus for reactivation later if

immuno compromised
Few - complications occur.
Especially if patient immune compromised
e.g. AIDS , malnourished children, elderly.
 Immunocompromised

unable to mount a CD4

reaction to maintain the organism

Progressive Primary Tuberculosis

Progressive primary tuberculosis

Resembles an acute bacterial pneumonia with

lower and middle lobe consolidation
hilar adenopathy
pleural effusion

Absence of the characteristic caseating

granulomas (nonreactive tuberculosis)
Complications

Lymphohaematogenous dissemination

tuberculous meningitis

miliary tuberculosis
Secondary/Post Primary/Reactivation
Tuberculosis

Occurs in a previously sensitized host

I.e. in an individual who has had primary

tuberculosis
 Occurs particularly when host resistance is
weakened.

May occur many decades after initial

infection.

May follow shortly after primary tuberculosis.

 Commonly it arises from reactivation of
dormant primary lesions.

It may also result from exogenous re infection

due to
- weakening of the protection afforded by the
primary disease.
- because of a large innoculum of virulent
bacilli.
 Primary Tuberculosis

< 5%

Secondary Tuberculosis
Secondary pulmonary tuberculosis is classically
localized to the apex of one or both upper lobes.
 This is thought to be due to the high oxygen
tension in the apices.

As a result of this localization, the regional

lymph nodes are less prominently involved
early in the developing disease than they are
in primary tuberculosis.
 pre existence of hypersensitivity

prompt and marked tissue response

to the bacilli

Walling off of the focus.

 Cavitation readily occurs in the secondary
form of TB

Erosion of the lesion into an airway

Person now raises sputum containing bacilli.

Secondary TB cavitation & scarring
 Localised secondary TB
asymptomatic
symptomatic

Symptoms

Insidious in onset due to

Low grade remittent fever Cytokine(TNF,IL1)
Night sweats release by
LOW, malaise macrophages
 With progressive pulmonary involvement
increasing amounts of sputum.
( mucoid purulent)

When cavitation is present, the sputum

contains tubercle bacilli.

Hemoptysis is present in about half of all cases

of pulmonary tuberculosis.
 Pleuritic pain may result from extension of the
infection to the pleural surfaces.
Extrapulmonary manifestations of tuberculosis
Depend on the organ system involved

tuberculous salpingitis infertility,

tuberculous meningitis headache and

neurologic deficits

Potts disease paraplegia

Complications of secondary TB
 Histologically, typical granulomas occur.

Progression of the disease depends on the

balance between host sensitivity and
organism virulence.

Most lesions are converted to fibrocalcific

scars.

As in primary TB, many complications can

ensue.
Miliary TB

May be a consequence of either primary or

secondary TB.

There is severe impairment of host resistance.

The disease becomes widely disseminated.

 Infective foci in the lungs

Organisms enter the pulmonary

venous circulation & enter the heart

Dissemination of organisms through the

systemic arterial system.

Seeding of multiple organs by the

organisms

Miliary Tuberculosis
 There are numerous small granulomas in
many organs
e.g. lungs, mining's ,kidneys, bone marrow,
liver, spleen

The granulomas often contain numerous

mycobacteria.
Miliary Tuberculosis of the Spleen
 The Mantoux test is frequently negative.

This is an acute medical emergency

necessitating prompt treatment with anti
tuberculous chemotherapy.

Otherwise the outcome may be fatal.

Mantoux Test

About 2 to 4 weeks after the infection

Intra cutaneous injection of 0.1 mL of PPD

Visible and palpable induration (at least 5 mm

in diameter) that peaks in 48 to 72 hours.
A positive tuberculin test result

Signifies cell-mediated hypersensitivity to

tubercular antigens.

It does not differentiate between infection and

disease.
False negative reactions (skin test anergy)

certain viral infections

sarcoidosis
malnutrition
Hodgkin's lymphoma
immunosuppression
overwhelming active TB.
False-positive reactions

infection by atypical mycobacteria.

 Sometimes, more PPD is required to elicit the
reaction.

In some responders, the standard dose may

produce a large, necrotizing lesion.
Diagnosis

1)Demonstration of acid-fast organisms in

sputum by acid-fast stains

most protocols require at least two sputum

examinations prior to conferring a diagnosis of
sputum negativity.
2)Cultures for mycobacteria

This requires up to 10 weeks.

This is the gold standard because it also allows
testing of drug sensitivity.
3) Liquid media-based radiometric assays

These detect mycobacterial metabolism

and are able to provide an answer within
2 weeks
4) PCR amplification of M. tuberculosis DNA

This allows for even greater rapidity of

diagnosis

PCR can detect as few as 10 organisms in

clinical specimens, compared with greater
than 10,000 organisms required for smear
positivity.
Prognosis

Infections localized to the lungs - Generally favorable

Prognosis worsens in,

the aged
debilitated
immunosuppressed (high risk for miliary tuberculosis)
and in those with multi drug resistant TB (MDR-TB)
Thank you