SEMINAR ON

pulmonary
tuberculosis

SUBMITTED TO;

MRS. JASMINE.P.V
LECTURER
BISHOP BENZIGER COLLEGE
OF NURSING, KOLLAM

SUBMITTED BY;

PARVATHY CHANDRAN
SECOND YEAR MSC NURSING
BISHOP BENZIGER COLLEGE
OF NURSING, KOLLAM

SUBMITTED ON; 08/05/17

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INTRODUCTION

Just a few years ago it was believed that TB was an old disease, and that it was no longer a
problem in humans. But now because of such issues as drug resistance and HIV, it has
become a major worldwide problem again. Worldwide more people die from the disease than
from any other infectious disease. TB is an abbreviation of the word Tuberculosis and is how
people often refer to the disease. It is caused by bacteria called Mycobacterium tuberculosis
(M. tuberculosis).

Tuberculosis (TB) is one of the most prevalent infections of human beings and contributes
considerably to illness and death around the world. It is spread by inhaling tiny droplets of
saliva from the coughs or sneezes of an infected person. It is a slowly spreading, chronic,
granulomatous bacterial infection, characterized by gradual weight loss. Tuberculosis (TB) is
an infectious disease usually caused by the bacterium Mycobacterium tuberculosis (MTB).
Tuberculosis generally affects the lungs, but can also affect other parts of the body. Most
infections do not have symptoms, in which case it is known as latent tuberculosis. About 10%
of latent infections progress to active disease which, if left untreated, kills about half of those
infected. The classic symptoms of active TB are a chronic cough with blood-
containing sputum, fever, night sweats, and weight loss. The historical term "consumption"
came about due to the weight loss. Infection of other organs can cause a wide range of
symptoms.

ANATOMY AND PHYSIOLOGY OF LUNGS

The lungs, which is the organ for respiration is a paired cone shaped organs lying in the
thoracic cavity separated from each other by the heart and other structures in the media
stinum. Each lung has a base resting on the diaphragm and an apex extending superiorly
to a point approximately 2.5 cm superior to the clavicle. It also has a medial surface and
with three borders- anterior, posterior and inferior. The broad coastal surface of the lungs
is pressed against the rib cage, while the smaller mediastinal surface faces medially. The
lung receives the bronchus, blood vessels, lymphatic vessels and nerves through a slit in
the mediastinal surface called the helium, and the structures entering the helium
constitutes the lungs root.

The right lung is larger and weighs more than the left lung. Since the heart tilts to the
left, the left lung is smaller than the right and has an indentation called the car diac
impression to accommodate the heart. This indentation shapes the inferior and anterior
parts of the superior lobe into a thin tongue-like process called the lingual.

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Pleura: Each lung is invested by and enclosed in a serous pleural sac that consists of two
continuous membranes. The visceral or pulmonary pleura invest the lungs, The parietal
pleura line the pulmonary cavities and adhere to the thoracic wall, mediastinum and
diaphragm.

The parietal pleura consist of four parts: coastal pleura which lines the internal surface of
the thoracic wall, mediastinal pleura which lines the lateral aspect of the mediastinum,
diaphragmatic pleura which lines the superior surface of the diaphragm on each side of
the mediastinum, cervical pleura extends through the superior thoracic aperture into the
root of the neck, forming a cup-shaped dome over the apex of the lung .

Pleural Cavity : The pleural cavity is the potential space between the visceral and
parietal layers of the pleural and it contains a capillary layer of serous pleural fluid
which lubricates the pleural surfaces and allows the layers to slide smoothly over each
other during respiration. Surface tension created by the pleural cavity provides the
cohesion that keeps the lung surface in contact with the thoracic wall.

Lobes and Fissures of the Lungs

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Each lung is divided into lobes by fissures. Both lungs have oblique fissure and the right
is further divided by a transverse fissure. The oblique fissure in the left lung separates
the superior and the inferior lobe. The oblique and horizontal fissure divides the lungs
into superior, middle and inferior lobes. Thus the right lung has three lobes while the left
has two. Each lobe is supplied by a lobar bronchus. The lobes are subdivided by
bronchopulmonary segments which are supplied by the segmental bronchi.
Bronchial Tree

All the respiratory passages from the trachea to the respiratory bronchioles are called the
tracheobronchial tree. The trachea divides at the sternal angle into right and left primary
bronchus which goes into the right and left lungs. Each bronchus enters the lung at a
notch called the hilum. Blood vessels and nerves also connect with the lungs here and
together with the bronchus forms a region called the root of the lungs.

The right main bronchus is larger in diameter and more vertical making it directly in line
with the trachea than the left main bronchus. Thus swallowed objects that accidentally
enter the lower respiratory tract are most likely to become lodged in the right main
bronchus.

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The main bronchi divide into lobar or secondary bronchi within each lung. Two lobar
bronchi exist in the left lung, and three exist in the right lung. The lobar bronchi, in turn
give rise to segmental or tertiary bronchi. The tertiary bronchi supply the
bronchopulmonary segments.

Bronchopulmonary Segment

Functionally, the lung is divided into a series of bronchopulmonary segments. The

bronchopulmonary segments are the largest subdivision of a lobe. They are separated
from adjacent segments by connective tissue septa and are also surgically resectable.
They are 10 bronchopulmonary segments in the left lung and 8-10 in the left lung.

The bronchi further divides, finally giving rise to the bronchioles which are less than
1mm in diameter. Each bronchioles divides into 50 to 80 terminal bronchioles, the final
branches of respiratory bronchioles. The functional unit of the lungs which is the acinus
includes the respiratory bronchioles, alveolar ducts, and sacs and the alveolar.
Approximately 16 generations of branching occur from the trachea to the terminal
bronchioles. As the air passageways of the lungs become smaller, the structure of their
walls changes.

Histology of Bronchopulomonary Segment

The major airways from the trachea through the ten generations of bronchi have
descending amounts of cartilaginous support surrounded by smooth muscles and elas tic
fibres, they have goblet cells for mucus production and are lined with ciliated columnar

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epithelium to facilitate secretion clearance. The next five generation of bronchioles have
no cartilage or goblet cells, but still have elastic tissue and smooth muscle fibres. They
lined with ciliated cuboidal epithelium. Relaxation and contraction of the smooth
muscles of the bronchi and bronchioles can change the diameter of the air passageways
and so change the volume of air moving through them. The alveoli provide a large
surface area for gas exchange. The alveolar walls consist of simple squamous epithelium.
Also the tissues surrounding the alveoli contain elastic fibres which allow the alveoli to
expand during inspiration and recoil during expiration.

The epithelium of the respiratory zone is not ciliated but debris from the air can be
removed by macrophages that move over the surface of the cells. Approximately 300
million alveoli are in the lungs. The average diameter of the alveoli is approximately
250um and their walls are extremely thin. There are two types of cells in the alveoli:
type I pneumocytes which are thin squamous epithelia cells that forms 90% of the alveoli
surface. Most of the gas exchange take place between these cells. Type II pneumocytes
are round secretory that produce surfactant, which makes it easier for the alveoli to
expand during inspiration.

Blood supply

The bronchial arteries arising from the aorta provide blood supply to the non -respiratory
airways, pleura, and connective tissue while the pulmonary arteries supply the
respiratory units (acini) and participate in gas exchange. Venous drainage is mainly by
the pulmonary veins (right and left superior and inferior pulmonary veins), though the
venous of drainage from the walls of the larger bronchi is carried out by the bronchial
veins. All four veins (pulmonary veins) drain into the left atrium.

Nerves supply

The lungs and airways are innervated by the branches of sympathetic trunk and vagus
nerve. Sympathetic nervous stimulation results in bronchodilation and slight
vasoconstriction, while parasympathetic nervous system stimulation results in
bronchoconstriction and indirect vasodilatation. The function of the lungs is controlled
through the respiratory centre with groups of neurons located at the pons and the medulla
oblongata, and complex interactions of specialized peripheral central chemoreceptors.

Relevance to Physiotherapy

Auscultation of the lungs and percussion of the thorax are important techniques used
during physical examination. Auscultation assesses airflow through the tracheobronchial
tree into the lungs.

Percussion helps establish whether the underlining tissues are air filled (resonant sound),
fluid filled (dull sound) or solid (flat sound).

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Based on the anatomy of the bronchial tree, gravity can be used to assist the clearance of
bronchial secretions through the use of positioning. Also Bronchial disorders such as
tumour and abscesses may be localized in a bronchopulmonary segments and may be
surgically removed without disrupting the surrounding lung tissue.

Defenses of the Lungs

There are a number of structures that protects the lungs from inhaled organisms and
particles:

 Nasal mucosa and hairs: warm and humidify inhaled air and filter out particle.
 Goblet cell and bronchial seromucous glands: produce mucous which contain
immunoglobulin A, cytokines, and other cytolytic substances, with extensive
mucosal production of nitric oxide by the nose and paranasal sinuses; all of these
have potent antimicrobial activity, to protect underlining tissues and trap organisms
and particles. Bacteria are destroyed by lysozyme in the mucus. Also additional
protection against bacteria is contributed by lymphocytes which populate the lamina
propria in large numbers. The lamina propria contains large blood vessels that help to
warm the air.
 Furthermore, the inferior concha has an especially large venous plexus called the
erectile tissue. Every 30 to 60 minutes, the erectile tissue on one side becomes
engorged and restricts air flow through that fossa, causing air to be redirected
through the other nostrils and fossa thus allowing the engorged side to time to
recover from drying. The flow of air shifts between the right and the left nostrils once
or twice each hour. Mucous production is increased by inflammation (e.g. in
conditions like asthma and bronchitis) and its composition can be altered by diseases.
 Cilia: structures move nucleus up the carina and the throat through mucocilliary
transport. Mucocilliary transport is impaired by inhalation of toxic gases (e.g.
cigarette smoke and air pollution), acute inflammation, infection, anesthesia, etc.
 Type II pneumocytes: produces surfactant which protects underlining tissue and
repairs damaged alveoli epithelium.

DEFINITION

Tuberculosis is the infectious disease caused by mycobacterium tuberculosis. It usually

involves the lungs, but it also occurs in the larynx, kidneys, bones, adrenal glands, lymph
nodes and meninges and can be disseminated throughout the body.

-Lewis

Tuberculosis is a potentially fatal contagious disease that can affect almost any part of the
body but is mainly an infection of the lungs. It is caused by a bacterial microorganism, the
tubercle bacillus/Mycobacterium tuberculosis.

-Medical Dictionary

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Tuberculosis is the infectious disease primarily affecting lung parenchyma is most often
caused by mycobacterium tuberculosis. It may spread to any part of the body including
meninges, kidney, bones and lymph nodes.

INCIDENCE

 2.3 million Die each year

 Global Emergency Tuberculosis kills 5,000 people a day
 It is currently estimated that 1/2 of the world's population (3.1 billion) is infected with
Mycobacterium tuberculosis
 With the increased incidence of AIDS, TB has become more a problem in the U.S.,
and the world.
 The highest incidence is seen in the developing countries of Africa and Asia.

ETIOLOGY

TB Spreads from person to person by airborne transmission. An infected persons releases

droplet nuclei (usually particles 1 to 5 Mm in diameter) through talking, coughing, sneezing,
laughing or singing. Larger droplets settle, smaller droplets remain suspended in the air and
are inhaled by a susceptible person.

 Exposure to TB
 Droplet nuclei (coughing, sneezing, laughing)
 Mycobacterium tuberculosis

RISKFACTORS

 Close contact with someone who has active tuberculosis.

Inhalation of airborne nuclei from an infected person is proportional to the amount of
time spent in the same air, space, the proximity of the person, and the degree of
ventilation.
 Immuno compromised status.
Those with HIV infection, cancer, transplanted organs and prolonged high dose
corticosteroids therapy.
 Drug abuse and alcoholism.
IV/injection drug users
 People lacking adequate health care.
The homeless, Impoverished, minorities, particularly children under age 15yrs and
young adults between ages 15 and 44yrs.
 Pre existing medical conditions
E.g. :( diabetes mellitus, chronic renal failure, malnourishment, selected malignancies,
haemodialysis, transplanted organs).
 Immigrants from countries with higher incidence of tuberculosis.
(South eastern Asia, Africa, Latin America, Caribbean)
 Institutionalisation (long term care facilities).
 Occupation (health care workers)

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  Living in substandard conditions
 Being a health care worker performing high risk activities.
 Institutionalization.
(Long term care facilities, Psychiatric institutions, prisons)

STAGES OF TUBERCULOSIS

First Stage:

 Droplet nuclei are inhaled, and are generated by talking, coughing and sneezing. Once
nuclei are inhaled, the bacteria are non-specifically taken up by alveolar macrophages.
 The macrophages will not be activated, therefore unable to destroy the intracellular
organism. The large droplet nuclei reaches upper respiratory tract and the small
droplet nuclei reach air sacs of the lung (alveoli) where infection begins. Disease
onset when droplet nuclei reach the alveoli.

Second stage:

 Begins after 7-21 days after initial infection. TB multiplies within the inactivated
macrophages until macrophages burst. Other macrophages diffuse from peripheral
blood, phagocytose TB and are inactivated, rendering them unable to destroy TB.

Third Stage:

 Lymphocytes, specifically T-cells recognize TB antigen. This results in T-cell

activation and the release of Cytokines, including interferon (IFN). The release of IFN
causes the activation of macrophages, which can release lytic enzymes and reactive
intermediates that facilitates immune pathology.
 Tubercle forms, which contains a semi-solid or “cheesy” consistency. TB cannot
multiply within tubercles due to low PH and anoxic environment, but TB can persist
within these tubercles for extended periods.

Fourth Stage

 Although many activated macrophages surround the tubercles, many other

macrophages are inactivated or poorly activated.
 The growing tubercle may invade a bronchus, causing an infection which may spread
to other parts of the lungs. Tubercle may also invade artery or other blood supply.
 Spreading of TB may cause milliary tuberculosis, which can cause secondary lesions.
Secondary lesions occur in bones, joints, lymph nodes, genitourinary system and
peritoneum.

Fifth Stage

 The caseous centers of the tubercles liquefy.This liquid is very crucial for the growth
of TB, and therefore it multiplies rapidly (extracellularly). This later becomes a large
antigen load, causing the walls of nearby bronchi to become necrotic and rupture.

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 This results in cavity formation and allows TB to spread rapidly into other airways
and to other parts of the lung.

TYPES

 Milliary tuberculosis / disseminated tuberculosis

 Bovine tuberculosis (mycobacterium bovis; of cattle)
 Avian tuberculosis (microbacterium avium; of birds)
 Pulmonary tuberculosis

TUBERCULOSIS CLASSIFICATION SYSTEM

The current clinical classification system for tuberculosis (TB) is based on the pathogenesis
of the disease. Health care providers should comply with local laws and regulations requiring
the reporting of TB. All persons with class 3 or class 5 TB should be reported promptly to the
local health department.
Classification System for TB

Class Type Description

No TB exposure No history of exposure

0
Not infected Negative reaction to tuberculin skin test

TB exposure
History of exposure
1 No evidence of
Negative reaction to tuberculin skin test
infection

Positive reaction to tuberculin skin test

TB infection
2 Negative bacteriologic studies (if done)
No disease
No clinical, bacteriologic, or radiographic evidence of TB

M. tuberculosis cultured (if done)

3 TB, clinically active Clinical, bacteriologic, or radiographic evidence of current
disease

History of episode(s) of TB
or
Abnormal but stable radiographic findings
TB
4 Positive reaction to the tuberculin skin test
Not clinically active
Negative bacteriologic studies (if done)
and
No clinical or radiographic evidence of current disease

5 TB suspect Diagnosis pending

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 TB disease should be ruled in or out within 3 months

PATHOPHYSIOLOGY

Initial infection or primary infection.

Entry of micro organism through droplet nuclei.

Bacteria are transmitted to alveoli through airways.

Deposition and multiplication of bacteria.

Bacilli are also transported to other parts of the body through blood stream and
phagocytosis by neutrophils and macrophages.

Accumulation of exudate in alveoli.

Broncho pneumonia.

New tissue masses of live and dead bacilli are surrounded by macrophages which form a
protective mass around granulomas.

Granulomas then transforms to fibrous tissue mass and central portion of which is
called ghon tubercle.

The material (bacteria and macrophages )becomes necrotic forming cheesy mass.

Mass becomes calcified and becomes colagenous scar.

Bacteria become dormant and no further progression of active disease.

Active disease or re infection.

Inadequate immune response.

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 Activation of dormant bacteria.

Ghon tubercle ulcerates and releasing cheesy material into bronchi.

Bacteria then become airborne resulting in further spread of infection.

Ulcerated tubercle heals and becomes scar tissue.

Infected lung become inflamed.

Further development of pneumonia and tubercle formation.

Unless the process is arrested it spreads downwards to the hilum of lungs and later
extends to adjascent lobes.

CLINICAL MANIFESTATIONS

We may not notice any symptoms of illness until the disease is quite advanced. Even then
the symptoms -- loss of weight, loss of energy, poor appetite, fever, a productive cough, and
night sweats -- might easily be blamed on another disease.

 Only about 10% of people infected with M. tuberculosis ever develop tuberculosis disease.
Many of those who suffer TB do so in the first few years following infection. However,
the bacillus may lie dormant in the body for decades.
 Although most initial infections have no symptoms and people overcome them, they may
develop fever, dry cough, and abnormalities that may be seen on a chest X-ray. This is
called primary pulmonary tuberculosis. Pulmonary tuberculosis frequently goes away by
itself, but in more than half of cases, the disease can return.
 Tuberculous pleuritis may occur in some people who have the lung disease from
tuberculosis.
 The pleural disease occurs from the rupture of a diseased area into the pleural space, the
space between the lung and the lining of the chest and abdominal cavities. This is often
quite painful since all of the pain fibers of the lung are located in the pleura.
 These people have a non-productive cough, chest pain, and fever. The disease may go
away and then come back at a later date.

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 In a minority of people with weakened immune systems, TB bacteria may spread through
their blood to various parts of the body.
 This is called miliary tuberculosis and produces fever, weakness, loss of appetite,
and weight loss.
 Cough and difficulty breathing are less common.
 Generally, return of dormant tuberculosis infection occurs in the upper lungs. Symptoms
include

 common cough with a progressive increase in production of mucus and

 Coughing up blood.

Other symptoms include the following:

 fever,
 loss of appetite,
 weight loss, and
 Night sweats.
 Some people may develop tuberculosis in an organ other than their lungs. About a quarter
of these people usually had known TB with inadequate treatment. The most common sites
include the following:

 Lymph nodes,
 Genitourinary tract,
 Bone and joint sites,
 Meninges, and
 The lining covering the outside of the gastrointestinal tract.

Constitutional symptoms

 Weight loss.
 Fatigue.
 Night sweats.
 Low grade fever.
 Anorexia.

Pulmonary symptoms

 Dyspnea
 Chest tightness

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  Non productive cough
 Mucopurulent sputum with hemoptpysis
 Chest Pain
 Non resolving bronchopneumonia

Extra pulmonary symptoms

 Pain.
 Inflammation.

Lymph node tuberculosis

Tuberculous lymphadenitis usually presents as painless swelling of one or more lymph nodes.
The nodes most commonly involved are those of the posterior or anterior cervical chain or
those in the supraclavicular fossa. Frequently the process is bilateral and other noncontiguous
groups of nodes can be involved. With continuing disease the nodes may become matted and
the overlying skin inflamed. Rupture of the node may result in formation of a sinus tract,
which is slow to heal. Intrathoracic adenopathy may compress bronchi, causing atelectasis
leading to lung infection and perhaps bronchiectasis being particularly common in children.

Pleural tuberculosis

There are two mechanisms by which the pleural space becomes involved in tuberculosis.
Early on a few organisms may gain access to the pleural space and, in the presence of cell-
mediated immunity, cause a hypersensitivity response. Commonly, this form of tuberculous
pleuritis goes unnoticed, and the process resolves spontaneously. In some this involvement of
the pleura is manifested as an acute illness with fever and pleuritic pain. If the effusion is
large, dyspnoea may occur but effusions generally are small and rarely bilateral. In
approximately 30% of patients there is no radiographic evidence of involvement of the lung
parenchyma even though parenchymal disease is nearly always present.

Genitourinary tuberculosis

It tends to present with local symptoms with systemic symptoms being less common.
Dysuria, hematuria and frequency of micturition are common. Flank pain may be noted.
However, often there is advanced renal destruction by the time of diagnosis. In women
genital involvement is more common without renal tuberculosis and may present with pelvic
pain, menstrual irregularities and infertility. In men a painless or only slightly painful scrotal
mass is probably the most common presenting symptom of genital involvement.

Skeletal tuberculosis

The usual presenting symptom is pain. Swelling of the involved joint may be noted with
limitation of motion and occasionally sinus tracts. Systemic symptoms of infection are not
common. Since the epiphyseal region of bones is highly vascularized in infants and young
children, bone involvement is much more common in these groups. Approximately 1% of
young children with tuberculosis will develop a bony focus. Delay in diagnosis can be
especially catastrophic in vertebral tuberculosis, where compression of the spinal cord may
cause severe and irreversible neurologic sequelae, including paraplegia. Early in the process
the only abnormality noted may be soft tissue swelling. The initial changes may be

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particularly difficult to detect by X-rays of the spine, but in advanced cases a fusiform
paravertebral abscess is visible. Computed tomographic (CT) scans and magnetic resonance
imaging (MRI) of are more sensitive and should be obtained when there is a high index of
suspicion of tuberculosis.

Central nervous system tuberculosis

Meningitis can result from direct meningeal seeding and proliferation during a tuberculous
bacillaemia either at the time of initial infection or at the time of breakdown of an old
pulmonary focus. It may result from breakdown of an old parameningeal focus with rupture
into the subarachnoid space. The consequences of subarachnoid space contamination are
diffuse meningitis or localized arteritis. In tuberculous meningitis the process is located
primarily at the base of the brain

Abdominal tuberculosis

Tuberculosis can involve any intra-abdominal organ and the peritoneum. The clinical
manifestations depend on the areas of involvement. Tuberculosis may occur in any location
from the mouth to the anus, although lesions proximal to the terminal ileum are unusual. The
most common sites of involvement are the terminal ileum and caecum. In the terminal ileum
or caecum the most common manifestations are pain, which may be misdiagnosed as
appendicitis or intestinal obstruction. A palpable mass may be noted that, together with the
appearance of the abnormality on barium enema or small bowel films can easily be mistaken
for a carcinoma. Rectal lesions usually present as anal fissures, fistulae or perirectal
abscesses.

Tuberculous peritonitis frequently presents with pain often accompanied by abdominal

swelling. Fever, weight loss, and anorexia are also common. The combination of fever and
abdominal tenderness in a person with ascites should always prompt an evaluation for intra-
abdominal infection and a paracentesis should be performed. However, this is often not
diagnostic, and laparoscopy with biopsy is recommended if tuberculosis is suspected.

Pericardial tuberculosis

The symptoms, physical findings, and laboratory abnormalities may be the result of either the
infectious process itself or the pericardial inflammation causing pain, effusion and eventually
hemodynamic effects. The systemic symptoms produced by the infection are nonspecific.
Fever, weight loss and night sweats are common. Cardiopulmonary symptoms tend to occur
later and include cough, dyspnea, orthopnea, ankle swelling and chest pain. The chest pain
may occasionally mimic angina but usually is described as being dull, aching, and affected by
position and inspiration. Apart from fever, the most common physical findings are those
caused by the pericardial fluid or fibrosis–cardiac tamponade or constriction. In the absence
of concurrent extracardiac tuberculosis, diagnosis of pericardial tuberculosis requires
aspiration of pericardial fluid or, usually, pericardial biopsy.

DIAGNOSTIC EVALUATION

History collection

Physical examination

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  Unusual breath sounds (crackles)
 Fluid around a lung (pleural effusion)
 Swollen or tender lymph nodes in the neck or other areas
 Clubbing of the fingers or toes (in people with advanced disease)

If Miliary tuberculosis; A physical exam may show:

 Swollen spleen
 Swollen lymph nodes
 Swollen liver

Tests may include:

 Tuberculin skin test (also called a PPD test)

 Thoracentesis.
 Sputum examination and cultures.
 Interferon-gamma release blood test such as the QFT-Gold test to test for TB
infection.
 Chest x-ray.
 Chest CT scan.
 Bronchoscopy.
 Biopsy of the affected tissue (rare).

TUBERCULIN SKIN TEST

0.1 Ml of PPD is injected forearm (sc).

After 48-72 hrs check for induration at the site.

Induration is equal to and more than 10mm.

Positive

The doctor will complete the following tests to diagnose tuberculosis. We may not be
hospitalized for either the initial tests or the beginning of treatment.

 Chest X-ray: The most common diagnostic test that leads to the suspicion of infection is a
chest X-ray. In primary TB, an X-ray will show an abnormality in the mid and lower lung
fields, and lymph nodes may be enlarged. Reactivated TB bacteria usually infiltrate the
upper lobes of the lungs. Miliary tuberculosis exhibits diffuse nodules at different
locations in the body.

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 The Mantoux skin test also known as a tuberculin skin test (TST or PPD test): This test
helps identify people infected with M. tuberculosis but who have no symptoms. A doctor
must read the test. The doctor will inject 5 units of purified protein derivative (PPD) into
your skin. If a raised bump of more than 5 mm (0.2 in) appears at the site 48 hours later,
the test may be positive. This test can often indicate disease when there is none (false
positive). Also, it can show no disease when you may in fact have TB (false negative).

 Quantiferon-TB Gold test: This is a blood test that is an aid in the diagnosis of TB. This
test can help detect active and latent tuberculosis. The body responds to the presence of the
tuberculosis bacteria. By special techniques, the patient's blood is incubated with proteins
from TB bacteria. If the bacteria are in the patient, the immune cells in the blood sample
respond to these proteins with the production of a substance called interferon-gamma
(IFN-gamma). This substance is detected by the test. If someone had a
prior BCG vaccination (a vaccine against TB given in some countries but not the U.S.) and
a positive skin test due to this, the QuantiFERON-TB Gold test will not detect any IFN-
gamma.

 Sputum testing: Sputum testing for acid-fast bacilli is the only test that confirms a TB
diagnosis. If sputum (the mucus you cough up) is available, or can be induced, a lab test
may give a positive result in up to 30% of people with active disease. Sputum or other
bodily secretions such as from your stomach or lung fluid can be cultured for growth of
mycobacterium to confirm the diagnosis. It may take one to three weeks to detect growth
in a culture, but eight to 12 weeks to be certain of the diagnosis.

When Should Someone Seek Medical Care for Tuberculosis?

If someone among our family or close associates is found to be sick with active TB, We
should see your doctor and be tested for tuberculosis.

 The dangerous contact time is before treatment. However, once treatment with drugs
starts, the sick person is non contagious within a few weeks.
 If we develop any side effects from medications prescribed to treat tuberculosis -- such as
itching, change in colour of skin, tiredness, visual changes, or excessive fatigue -- call our
doctor immediately.

Drug-Resistant TB

 Most strains of the TB bacteria require at least two drugs for treatment to prevent
resistance.
 Resistance is caused by inconsistent or partial treatment. In some instances, patients are
prescribed inadequate therapy or enough drugs are not available. Usually this occurs
because patients tend to stop taking their medication once they start to feel better.
Observed therapy is often required and monitored by health departments in the U.S.
 Multidrug-resistant TB (MDR-TB) is caused by bacteria that are resistant to at least
isoniazid and rifampicin. Prolonged alternative therapy is required to treat this form of TB,
often for up to two years.

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 Extensively drug-resistant TB (XDR-TB) is rare but extremely problematic. This form of
TB is very difficult to treat and often requires prolonged isolation of the individual to
protect the community at large. If TB is treated properly and consistently, these resistant
forms are much less likely to spread.

MEDICAL MANAGEMENT

PULMONARY TB is treated primarily with antituberculosis agents for 6 to 12 months.

Pharmacological management

First line antitubercular medications

 Streptomycin 15mg/kg
 Isoniazid or INH(Nydrazid) 5 mg/kg(300 mg max per day)
 Rifampin 10 mg/kg
 Pyrazinamide 15 – 30 mg/kg
 Ethambutol (Myambutol) 15 -25 mg/kg daily for 8 weeks and continuing for up to 4
to 7 months.

Second line medications

 Capreomycin 12 -15 mg/kg

 Ethionamide 15mg/kg
 Para aminosalycilate sodium 200 300 mg/kg
 Cycloserine 15 mg/kg
 Vitamin b (pyridoxine) usually administered with INH

Other drugs that may be useful, but are not on the WHO list of SLDs

 Rifabutin
 Macrolides:e.g.,clarithromycin (CLR)
 Linezolid(LZD)
 Thioacetazone(T)
 Thioridazine
 Arginine

First line drugs: - kill active bacteria, important in the early stages of infection.

Second line drugs: - hinder bacterial growth. - Strengthen treatment in the case of resistant
bacteria. - Less efficient and generally more toxic than first line drugs.

ISONIAZIDE (H):

 Is the most active drug.

 It’s structurally similar to pyrodoxine.
 Bactericidal for fast growing bacteria.
 Is able to penetrate into phagocytic cells & thus active against both extracellular &
intracellular.

18
  Less effective against atypical mycobacterium.

Mechanism of action

 Inhibits synthesis of Mycolic acid.

 It’s a pro drug activated by KatG.
 Resistance to INH is associated with over expression of inhA.
 Overproducers of inhA express low level INH resistance & cross resistance to
ethionamide.
 KatG mutant’s express high level of INH resistance & usually no cross resistance to
ethionamide.

Pharmacokinetics

 INH is readily absorbed from GIT.

 INH readily diffuses in all body fluids.
 Peak plasma concentration of 3-5µg/ml within 1-2 hrs.
 Half life is about 1-3 hrs.

Dosage

 5mg/kg/day once daily.

 Up to 10 mg/kg/day can be used if malabsorption is not an issue.
 High dose upto 15mg/kg/day twice a week.

Side effects

 Rash
 Abnormal liver function
 Anemia,
 Peripheral neuropathy
 Mild CNS effects

RIFAMPIN(R)

 It’s a semi-synthetic derivative of rifamycin, antibiotic produced by streptomycin

mediterranei.
 Active against gram + & -ve, some enteric, mycobacterium & Chlamydia.
 There is no cross resistance to other class of anti microbials but there is a cross
resistance to other rifamycin derivatives.

Moa & Pharmacokinetics

 Inhibits RNA synthesis.

 Resistance is from mutation in rpoB gene.
 Human RNA polymerase does not binds with Rifampin.
 Rifampin is bactericidal for mycobacteria.
 Its excreted mainly through liver so dosage adjustment in renal failure is not required.

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  Rifampin is highly protein bound.CSF concentration is achieved only in presence of
meningeal inflammation.

Side effects

 Fever
 Immune reactions
 GI irritation
 Liver damage
 Can cause tears and urine to turn red/orange

Clinical usage

Dosage: - 10 mg/kg/day

Oral dosage of 600mg twice daily from 2 days to eliminate meningococcal carriage.

ETHAMBUTOL (E)

 Synthetic water soluble ,heat stable compound.

 Inhibits mycobacterial arabinosyl transferase.
 Ethambutol accumulates in renal failure.
 Crosses the blood brain barrier only if the meninges are inflamed.
 Mutation to ethambutanol is due to mutation in over expression of emb Gene products
or with embB structral gene.
 Resistance to ethambutol emerges rapidly if the drug is used alone.

Clinical usage

 Dosage:-15-25mg/kg as a single dose.

 Higher doses are recommended for tuberculos meningitis.
 Dosage is 50 mg/kg when twice weekly schedule is followed.
 Bacteriostatic.

Side effects

 Decrease in visual acuity

 Colour blindness and other visual defects
 Joint pain
 Nausea
 Vomiting
 Fever, malaise
 Headache
 Dizziness

PYRAZINAMIDE (Z)

 At neutral p H it is inactive invitro whereas at p H 5.5 it inhibits tuberculi bacilli.

20
  Drug acts against intracellular organism.
 Drug is converted into PYRAZINOIC ACID, active form of drug by pyrazinamidase.
 Encoded by pncA.
 Resistance is due to mutation in pncA which impairs conversion of pyrazinamide in
active form & impair its uptake.

Clinical usage

 Half life is 8-11 hrs.

 Dosage: 50-70 mg/kg/d for twice / thrice weekly treatment regimens.
 Bactericidal & bacteriostatic.

Side effects

 Bactericidal Joint pain

 Nausea
 Vomiting
 Rash
 Malaise
 Fever
 Photosentivity

STREPTOMYCIN(S)

 Active mainly against extracellular.

 Source: Streptomyces griseus.
 First line Anti TB drug, given by injection Pharmacokinetics:
 Penetrates into cells poorly & ineffective for intracellular tubercle bacilli.
 Crosses BBB & achieves therapeutic conc. if meninges are inflamed

Mechanism of action

 Streptomycin binds to 12 S ribosomal sub units. Irreversible Inhibition of protein

synthesis by: Interference with initiation complex of peptide formation.
 Misreading of code on mRNA --- incorporation of incorrect Amino acid into the
peptide chain, resulting in non- functional or toxic protein.
 Inhibition of translocation.
 Break up of polysomes into non functional monosomes.
 These activities occur simultaneously & overall effect is lethal for the cell.

Side effects

 Damage to the ears

 Nausea
 Rash
 Vomiting
 Vertigo

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THIACETAZONE (Tzn)

 Bacteriostatic drug.
 Does not add the therapeutic effect to the H, S& Z but delays resistance to these
drugs.
 Half life is 12 hrs.
 Major adverse effects is hepatitis, exfoliative dermatitis, Stevens- Jonson syndrome.
 Tzn is not used in HIV patients due to incidence of serious toxicity.
 Dosage: - 150 mg/d in adults & 2.5mg/kg in children.

ETHIONAMIDE (Etm)

 Bacteriostatic drug.
 Acts on both extra & intracellular organism.
 Resistance to Etm develops rapidly.
 Cross resistance with Tzm is also seen.
 Half life is 2-3 hrs.
 Recommended dosage is 1g/d.
 Anorexia, nausea & abdominal complaints are common.

CYCLOSERINE (Cys)

Obtained from S.ORCHIDACEUS.

 Inhibits bacterial wall synthesis.

 Bacteriostatic drug.
 Rarely used.
 Dosage :- 250 mg /B.D if tolerated can be increased to 500 mg B.D

ANTITUBERCULAR DRUG REGIMEN

1. Standard regimens:

Anti-TB drugs are given as 2/3/4 drug combination regimens for different durations.
Combination regimen should include at least two drugs to which mycobacteria are sensitive.
The response to chemotherapy is slow so given for months to years. Standard regimens: May
be given in two phases.

i. Initial Intensive Phase for 2 months

ii. Continuation Phase for 4 months

Initial Intensive Phase for 2 months:

Therapy is initiated with 4 drug regimen. Isoniazid , Rifampin , Pyrazinamide & Ethambutol
or Streptomycin.– Neither Ethambutol nor Streptomycin decreases the duration of the
regimen, but they provide additional coverage for mycobacterium if isolate proves to be
resistant to Isoniazid / Rifampin or to both.

22
Continuation Phase for 4 months:

 A few bacilli are left; only 2/ 3 drugs are enough.

 Isoniazid and Rifampin
 Isoniazid, Rifampin, Pyrazinamide / Ethambutol
 Pyridoxine: 25 to 50mg/day, to minimize adverse reactions to isoniazid. Standard
regimen may be given as DOTS
 Recommended by WHO in 1995. For noncompliant patient

2. Alternative regimens:

 Alternative regimens for fully susceptible organisms include: INH + Rifampin for 9
months
 INH + Ethambutol for 18 months.
Intermittent (2 or 3 x weekly) high dose 4 drug regimens are also effective.

DOTS (DIRECTLY OBSERVED TREATMENT, SHORT-COURSE)

DOTS are the name given to the World Health Organization-recommended tuberculosis
control strategy that combines five components:

1. Government commitment (including both political will at all levels, and establishing a
centralized and prioritized system of TB monitoring, recording and training).

2. Case detection by sputum smears microscopy.

3. Standardized treatment regimen directly observed by a healthcare worker or community

health worker for at least the first two months.

4. A regular drug supply.

5. A standardized recording and reporting system that allows assessment of treatment results

DOT is especially critical for patients with drug resistant TB, HIV-infected patients, and
those on intermittent treatment regimens (i.e., 2 or 3 times weekly).

MULTIPLE-DRUG THERAPY

Multiple-drug therapy to treat TB means taking several different antitubercular drugs at the
same time.

The standard treatment is to take isoniazid, rifampin, ethambutol, and pyrazinamide for 2
months. Treatment is then continued for at least 4 months with fewer medicines.

NURSING ASSESSMENT

Assessment

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  Obtain history of exposure to TB.
 Assess for symptoms of active disease.
 Auscultate lungs for crackles.
 During drug therapy assess for liver function.

Nursing Diagnosis

1. Ineffective breathing pattern related to pulmonary infection and potential for long term
scarring with decreased lung capacity.

Interventions

 Instruct about best position to facilitate drainage.

 Encourage increased fluid intake.
 Provide supplemental oxygen as ordered.
 Monitor breath sounds respiratory rates, sputum production and dyspnoea.
 Encourage rest and avoidance of exertion.
 Administer and teach self administration of medications ordered.

2. Risk for spreading infection related to nature of disease and patients symptoms

Interventions

 Carefully monitor vital signs and observe for temperature changes.

 Instruct about risk of drug resistance if drug regimen is not strictly and continuously
followed
 Isolation of patient.
 Educate patient to control the spread of infection by covering mouth and nose while
coughing and sneezing.
 Use high efficiency particulate masks for high risk procedures including endoscopy.
 Be aware that TB is transmitted by respiratory droplets.

3. Imbalanced nutrition less than body requirement related to poor appetite, fatique and
productive cough.

Interventions

 Administer vitamin supplements as ordered.

 Monitor weight of the patient.
 Provide small frequent meals.
 Explain the importance of eating nutritious diet to promote healing and defense
against infection.

4. Non compliance related to lack of motivation and lack of treatment.

Interventions

 Instruct about medications schedule and side effects.

24
  Explain that TB is a communicable disease and that taking medications is most
effective way of preventing transmission.
 Participate in observation of medicine taking, weekly pill counts or programmes
designed to increase compliance with the treatment for TB
 Review adverse effects of drug therapy.
 Educate patient about etiology transmission and effects of TB.

PREVENTION

If the test positive for latent TB infection, doctor may advise to take medications to
reduce the risk of developing active tuberculosis. The only type of tuberculosis that is
contagious is the active variety, when it affects the lungs. So if we can prevent the latent
tuberculosis from becoming active, we won't transmit tuberculosis to anyone else.

Protect our family and friends

If we have active TB, keep our germs to ourself. It generally takes a few weeks of
treatment with TB medications before we are not contagious anymore. Follow these tips
to help keep your friends and family from getting sick:

 Stay home. Don't go to work or school or sleep in a room with other people during
the first few weeks of treatment for active tuberculosis.

 Ventilate the room. Tuberculosis germs spread more easily in small closed spaces
where air doesn't move. If it's not too cold outdoors, open the windows and use a
fan to blow indoor air outside.

 Cover our mouth. Use a tissue to cover our mouth anytime we laugh, sneeze or
cough. Put the dirty tissue in a bag, seal it and throw it away.

 Wear a mask. Wearing a surgical mask when we are around other people during
the first three weeks of treatment may help lessen the risk of transmission.

Finish our entire course of medication

This is the most important step we can take to protect ourself and others from tuberculosis.
When we stop treatment early or skip doses, TB bacteria have a chance to develop mutations
that allow them to survive the most potent TB drugs. The resulting drug-resistant strains are
much more deadly and difficult to treat.

25
Vaccinations

In countries where tuberculosis is more common, infants often are vaccinated with bacillus
Calmette-Guerin (BCG) vaccine because it can prevent severe tuberculosis in children. The
BCG vaccine isn't recommended for general use in the United States because it isn't very
effective in adults. Dozens of new TB vaccines are in various stages of development and
testing.

Home treatment for tuberculosis(TB) focuses on taking the medicines correctly to reduce the
risk of developing multidrug-resistant TB.

 Keep all your medical appointments.

 Take our medicines as prescribed.
 Report any side effects of the medicines, especially vision problems.
 If we plan to move during the time that we are being treated, let our doctor know so
that arrangements can be made for you to continue the treatment.

Healthy eating and exercise

During treatment for TB, eat healthy foods and get enough sleep and some exercise to help
our body fight the infection.
If we are losing too much weight, eat balanced meals with enough protein and calories to
help we keep weight on. If we need help, ask to talk with a registered dietitian.
Assess the Symptoms

 If we do not feel like eating, eat our favourite foods. Eat smaller meals several times a
day instead of a few large ones.
 Drink high-calorie protein shakes between meals. Or try nutritious drinks, such as
Ensure.
 If we feel sick to our stomach, try drinking peppermint or ginger tea.
 Ask our doctor when it is safe for to exercise. When we can go outside, walking is
good way to get exercise. Start slowly if we have not been active. Try one 20-minute
or two 10-minute walks to start. Slowly increase our time. Try to walk as often as we
can.

Emotional issues
Because TB treatment takes so long, it is normal to:

 Be embarrassed about having TB and worried that other people will find out about it.
 Feel bad because people have to wear a mask to keep from getting infected when they
are near.
 Feel isolated and alone because cannot go to work, school, or public places until we
can no longer infect other people.
 Be worried about losing income or losing our job during treatment. We may also
worry about paying for our medicines and doctor visits.

26
  Feel guilty about the stress this is causing to family members or friends who are
worried about getting TB or already have it.
 Feel depressed.

Home treatment for tuberculosis (TB) focuses on taking the medicines correctly to reduce the
risk of developing multidrug-resistant TB.

 Keep all our medical appointments.

 Take our medicines as prescribed.
 Report any side effects of the medicines, especially vision problems.
 If we plan to move during the time that we are being treated, let our doctor know so
that arrangements can be made for we to continue the treatment.

Healthy eating and exercise

During treatment for TB, eat healthy foods and get enough sleep and some exercise to help
our body fight the infection.
If we are losing too much weight, eat balanced meals with enough protein and calories to
help we keep weight on. If we need help, ask to talk with a registered dietitian.

Protecting others

 Don't go to work or school while we can spread the TB infection. Sleep in a bedroom by
yourself until we can no longer infect other people.
 Open windows in a room where we must stay for a while, if the weather allows it. This
can help get rid of TB bacteria from the air in the room.
 Cover our mouth when we sneeze or cough. Until we have been on antibiotics for about 2
weeks, we can easily spread the disease to others. After coughing, dispose of the soiled
tissue in a covered container. Talk with our doctor about other precautions we can take to
prevent the spread of TB.

COMPLICATIONS

 Bones: Spinal pain and joint destruction may result from TB that infects your bones
(TB spine or potss spine)
 Brain: Meningitis
 Liver or kidneys
 Heart: Cardiac tamponade
 Pleural effusion
 Tb pneumonia
 Serious reactions to drug therapy (hepato toxicity; hypersentivity)

27
EVIDENCE BASED PRACTICE

1. VALIDATION OF EVIDENCE-BASED CLINICAL PRACTICE GUIDELINE:

NURSING INTERVENTION FOR NEWLY DIAGNOSED PULMONARY

TUBERCULOSIS PATIENTS AT COMMUNITY SETTING

Author links open overlay panelAmel IbrahimAhmedSahar MohamedSolimanLamiaa
AminAwad

Abstract

Background

Tuberculosis is a major contributor to disease burden in the developing countries. It is

considered the second fatal disease all over the world and the third most important public
health problem in Egypt. The direct causes of increasing the burden of tuberculosis are the
inconsistent and fragmented health services. The nursing interventions of tuberculosis in
community settings require a system of recommendations that ensure the consistency of care.

Objective

The present study aimed at providing a valid evidence-based clinical guideline that assists
nurses to intervene consistently to the newly diagnosed patient with pulmonary tuberculosis.

Methods

The intended guideline was developed according to the criteria of the Scottish Intercollegiate
Guidelines Network (SIGN) and the American Academy of Neurology. This guideline was
developed based on the need for assessments of the intended users (nurses) and the end-point
beneficiaries (newly diagnosed patients with pulmonary tuberculosis). The development
process of the guideline consisted of seven main steps. The SIGN appraisal tools were used
for the critical appraisal phase of the retrieved studies, and the “Appraisal of Guidelines for
Research & Evaluation (AGREE) Instrument” that was used for appraising the internal
validity of the developed guideline.

Results

The developed guideline included thirty recommendations categorized into four main themes,
which are assessment, nursing diagnosis, nursing care plan and implementation of care plan.
The overall assessment of the guideline revealed that two-thirds of academic appraisers
strongly recommended the guideline to be used in practice and most of practitioner nurses
and practitioner physicians recommended the guideline to be in practice.

28
Conclusion

The development of this guideline was based on the needs of the targeted users (nurses) and
end-point beneficiaries (patients). It was strongly recommended by the appraisers to be used
in the outpatient’s chest clinics. The study recommended that this developed guideline should
be disseminated to the policy makers to be approved for application.

2. NEW CLINICAL PRACTICE GUIDELINES ON DIAGNOSIS OF

TUBERCULOSIS IN ADULTS AND CHILDREN

New Clinical Practice Guidelines on Today, ATS, CDC and IDSA published their official
clinical guideline on TB diagnosis. Madhukar Pai

Dec 09, 2016

Diagnosis remains one of the weakest links in tuberculosis care and control. Today, a
new guideline was published in Clinical Infectious Diseases. A task force, to which I
contributed, supported by the American Thoracic Society, Centers for Disease Control and
Prevention, and Infectious Diseases Society of America searched, selected, and synthesized
relevant evidence. The evidence was then used as the basis for recommendations about the
diagnosis of tuberculosis disease and latent TB infection (LTBI) in adults and children. The
recommendations were formulated, written, and graded using the GRADE approach. 23
evidence-based recommendations about diagnostic testing for latent tuberculosis infection,
pulmonary tuberculosis, and extra pulmonary tuberculosis are provided. Six of the
recommendations are strong, whereas the remaining 17 are conditional.

3. VALIDATION OF EVIDENCE-BASED CLINICAL PRACTICE GUIDELINE:

NURSING INTERVENTION FOR NEWLY DIAGNOSED PULMONARY
TUBERCULOSIS PATIENTS AT COMMUNITY SETTING

Abstract

Background: Tuberculosis is a major contributor to disease burden in the developing

countries. It is considered the second fatal disease all over the world and the third most
important public health problem in Egypt. The direct causes of increasing the burden of
tuberculosis are the inconsistent and fragmented health services. The nursing interventions of
tuberculosis in community settings require a system of recommendations that ensure the
consistency of care. Objective: The present study aimed at providing a valid evidence-based
clinical guideline that assists nurses to intervene consistently to the newly diagnosed patient
with pulmonary tuberculosis. Methods: The intended guideline was developed according to
the criteria of the Scottish Intercollegiate Guidelines Network (SIGN) and the American

29
Academy of Neurology. This guideline was developed based on the need for assessments of
the intended users (nurses) and the end-point beneficiaries (newly diagnosed patients with
pulmonary tuberculosis). The development process of the guideline consisted of seven main
steps. The SIGN appraisal tools were used for the critical appraisal phase of the retrieved
studies, and the ‘‘Appraisal of Guidelines for Research & Evaluation (AGREE) Instrument’’,
that was used for appraising the internal validity of the developed guideline.

4. PROMOTING ADHERENCE TO TREATMENT FOR TUBERCULOSIS: THE

IMPORTANCE OF DIRECT OBSERVATION
Thomas R Frieden, John A Sbarbaro
Since 1993, WHO has recommended a strategy through which national governments can
meet their responsibility to treat patients and to prevent the spread of tuberculosis (TB)
Four of the major elements of the strategy, which came to be known as DOTS, were
political commitment by governments, improved laboratory services, a continuous supply
of good-quality drugs, and a reporting system to document the progress (and failure) of
treatment for individual patients and of the programme. The fifth element, effective case
management via direct observation of treatment by an independent and trained third party,
was a response to decades of reports documenting the failure of patients to complete
treatment. Put simply: direct observation of treatment is an integral and essential
component of DOTS.
WHO has reported that more than 30 million patients with TB have been treated with its
five-element DOTS strategy, resulting in cure rates of > 80% and default rates of <
10%.WHO’s recently announced Global Plan to Stop TB highlights the need to expand
DOTS through “standardized treatment, under proper case management conditions,
including directly observed treatment to reduce the risk of acquiring drug resistance, and
support of patients to increase adherence to treatment and chance of cure”.
However, the value of the direct observation component of DOTS has been questioned in
a recent systematic review, in which it was suggested that direct observation of treatment
is unnecessary and disrespectful of patients. Both self-administered treatment and
treatment observation by a family member have been proposed as acceptable alternatives.
We challenge the validity of these assertions.

5. EVIDENCE-BASED INTERVENTIONS FOR DIAGNOSING, PREVENTING AND

TREATING TUBERCULOSIS MAY 2014

Introduction Tuberculosis occurs all over the world, particularly in poorer regions, and where
human immunodeficiency virus (HIV) is common. Over 95% of tuberculosis deaths occur in
developing countries and it is among the top three causes of death for women between the
ages of 15-44. This booklet provides summaries of Cochrane systematic reviews for the
diagnosis, prevention and treatment of tuberculosis. What is a Cochrane systematic review?
A Cochrane systematic review asks a specific research question about a particular healthcare
intervention in a clearly defined group of people with a health condition or problem; for
example does isoniazid prevent Tuberculosis in non-infected HIV persons. These reviews
summarise the results of healthcare studies and provides the evidence on the effectiveness of
the interventions. These reviews are produced by The Cochrane Collaboration and it is

30
published in an online database, The Cochrane Library (www.thecochranelibrary.com) The
South African Cochrane Cent

Summary

Tuberculosis (TB) is a serious bacterial infection and it is estimated that about a third of the
world's population is infected with TB. There are a number of types, such as pulmonary TB
(bacteria residing in a person's lungs) and spinal TB (in the spine). Some bacteria can be drug
resistant and some people may have the infection alongside another medical condition.
People suffer from severe cough, weakness and sweats, and some people still die from TB
even though effective drug treatment has been around for many years. The incidence of TB
has reduced in areas where the drugs are readily available. Preventing people from
contracting TB in high-risk areas is a goal worth pursuing. The review of trials using
isoniazid for a six- to 12-month period in people without HIV infection (HIV infected people
were studied in another review) identified 11 trials involving over 90,000 people. Isoniazid
was effective in preventing TB in 60% of people, although some did develop hepatitis. The
findings showed that one person can be saved from getting TB when 35 people take isoniazid
for six months, and one in every 200 treated will get hepatitis. The balance of benefits and
harms need to be carefully considered for each setting where intervention is being considered.

31
SUMMARY

The bacterium Mycobacterium tuberculosis causes tuberculosis (TB), a contagious, airborne

infection that destroys body tissue. Pulmonary TB occurs when M. tuberculosis primarily
attacks the lungs. However, it can spread from there to other organs. Pulmonary TB is curable
with an early diagnosis and antibiotic treatment. Pulmonary TB, also known as consumption,
spread widely as an epidemic during the 18th and 19th centuries in North America and
Europe. After the discovery of antibiotics like streptomycin and especially isoniazid, along
with improved living standards, doctors were better able to treat and control the spread of TB.
Since that time, TB has been in decline in most industrialized nations. However, TB remains
in the top 10 causes of death worldwide, according to the World Health Organization (WHO),
with an estimated 95 percent of TB diagnoses as well as TB-related deaths occur in
developing countries. That said, it’s important to protect ourself against TB. Over 9.6 million
people have an active form of the disease, according to the American Lung Association
(ALA). If left untreated, the disease can cause life-threatening complications like permanent
lung damage.

32
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Kluwer pvt ltd; 2009.
4. Holler T. Cardiology Essentials. 1st ed. Canada: Jones and Barlett publishers; 2008.
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Brothers Medical Publishers; 2016.

Journal

1. Validation of evidence-based clinical practice guideline: nursing intervention for

newly diagnosed pulmonary tuberculosis patients at community setting
2. New clinical practice guidelines on diagnosis of tuberculosis in adults and children

3. Validation of evidence-based clinical practice guideline: nursing intervention for

newly diagnosed pulmonary tuberculosis patients at community setting

4. Promoting adherence to treatment for tuberculosis: the importance of direct

observation
5. Evidence-based interventions for diagnosing, preventing and treating tuberculosis
may 2014

Web

1. www.pubmed.com
2. www.wikipedia.com
3. www.medline plus.com

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