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CASE STUDY:

PULMONARY
TUBERCULOSIS
ACTIVE TUBERCULOSIS
INTRODUCTION
Tuberculosis is a highly prevalent chronic infectious disease caused by
Mycobacterium tuberculosis bacilli. Globally Mycobacterium tuberculosis infection
remains at an epidemic level affecting one third of world population. About 1 million
Filipinos have active TB disease. This is the third highest prevalence rate in the
world, after South Africa and Lesotho. It is a highly curable disease. Yet, it is the
number one killer among all infectious diseases. Every day more than 70 people lose
their lives to TB in the Philippines needlessly. the emergence of human
immunodeficiency virus (HIV) infection has made the situation worse.2 Around 10%
of tuberculosis cases are in the first and second decade of life. It affects three times as
many men as women

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
INTRODUCTION

Tuberculosis is an infectious disease that primarily affects the lung parenchyma.


It also may be transmitted to other parts of the body, including the meninges, kidneys,
bones, and lymph nodes.
The primary infectious agent, M. tuberculosis, is an acid-fast aerobic rod that grows
slowly and is sensitive to heat and ultraviolet light.
Although current research in the past four years has provided valuable insight into TB
transmission, diagnosis, and treatment, much remains to be discovered to effectively
decrease the incidence of and eventually eradicate TB. The disease still puts a strain
on public health, being only second to HIV/AIDS in causing high mortality rates. 
FINDINGS
2019 WHO Global TB Report
PREVALENCE
(Cohort of 2018)
Newly infected
Mortality 24/100,000 Incidence 554/100,000
1,000,000,000
Total Notified Cases: 382,543 Active

Treatment Coverage: 63%


382,543
Diagnosed
Treatment Success Rate, All Forms (2017) : 91% 200,000,000

35,000,000
will die of TB Tuberculosis IF NO
early detection and treatment
Etiology

● Infection with Mycobacterium tuberculosis (alcohol and acid-fast bacillus)


causes active tuberculosis. It is classified under the M. tuberculosis complex
group, which includes four other mycobacteria that can cause active
tuberculosis: M. canettii, M. microti, M. bovis, and M. africanum.

● M. tuberculosis is an obligate-aerobic, nonmotile, non-spore-forming,


catalase-negative, and facultative intracellular bacteria. The high lipid
content of M. tuberculosis gives it many unique clinical characteristics.
These include resistance to several antibiotics and the ability to survive in
many extreme conditions. It also takes a long time to divide (around 16 to 20
hours), a significantly slower rate compared to other bacteria, which usually
takes less than an hour.
Etiology

● The organism has a poor reaction to Gram stain and, thus, is not classified as
gram-positive or gram-negative. However, sometimes weakly positive cells
are observed on Gram stain, referred to as “ghost cells.” As M. tuberculosis
retains some stains even after being treated with solutions containing acids,
hence it is considered an acid-fast bacillus. The Ziehl-Neelsen stain and the
Kinyoun stain are most commonly used to identify M. tuberculosis. The test
dyes the acid-fast bacilli bright red, which makes it distinct against a blue
background.

● Humans are the only known host in which M. tuberculosis naturally lives
and reproduces. The organism is spread primarily as an airborne aerosol
from an individual in the infectious stage of the disease, although
transdermal and gastrointestinal (GI) transmission is also possible.
Signs and Symptoms

S.N BOOK PICTURE


1. Breathing difficulty

2. Chest pain

3. A cough that lasts more than 3 weeks

4. Cough with blood and/or with phlegm

5. Fatigue

6. Fever

7. Night sweats

8. Weakness

9. Weight loss

10. Wheezing
PHYSICAL
EXAMINATION
ANATOMY AND PHYSIOLOGY
The lungs are pyramid-shaped, paired organs that are connected to the
trachea by the right and left bronchi; on the inferior surface, the lungs are
bordered by the diaphragm. The diaphragm is the flat, dome-shaped
muscle located at the base of the lungs and thoracic cavity. The lungs are
enclosed by the pleurae, which are attached to the mediastinum. The
right lung is shorter and wider than the left lung, and the left lung
occupies a smaller volume than the right. The cardiac notch is an
LUNGS indentation on the surface of the left lung, and it allows space for the
heart. The apex of the lung is the superior region, whereas the base is the
opposite region near the diaphragm. The costal surface of the lung
borders the ribs. The mediastinal surface faces the midline.
ANATOMY AND PHYSIOLOGY
Each lung is composed of smaller units called lobes. Fissures separate
these lobes from each other. The right lung consists of three lobes: the
superior, middle, and inferior lobes. The left lung consists of two lobes:
the superior and inferior lobes. A bronchopulmonary segment is a
division of a lobe, and each lobe houses multiple bronchopulmonary
segments. Each segment receives air from its own tertiary bronchus and
is supplied with blood by its own artery. Some diseases of the lungs
typically affect one or more bronchopulmonary segments, and in some
cases, the diseased segments can be surgically removed with little
influence on neighboring segments. A pulmonary lobule is a subdivision
formed as the bronchi branch into bronchioles. Each lobule receives its
own large bronchiole that has multiple branches. An interlobular septum
is a wall, composed of connective tissue, which separates lobules from
one another.
ETIOLOGY
Infection with Mycobacterium tuberculosis (alcohol and acid-fast bacillus) causes active tuberculosis. It is classified
under the M. tuberculosis complex group, which includes four other mycobacteria that can cause active
tuberculosis: M. canettii, M. microti, M. bovis, and M. africanum.

M. tuberculosis is an obligate-aerobic, nonmotile, non-spore-forming, catalase-negative, and facultative intracellular


bacteria. The high lipid content of M. tuberculosis gives it many unique clinical characteristics. These include
resistance to several antibiotics and the ability to survive in many extreme conditions. It also takes a long time to
divide (around 16 to 20 hours), a significantly slower rate compared to other bacteria, which usually takes less than
an hour. As M. tuberculosis retains some stains even after being treated with solutions containing acids, hence it is
considered an acid-fast bacillus. The Ziehl-Neelsen stain and the Kinyoun stain are most commonly used to identify
M. tuberculosis.

Humans are the only known host in which M. tuberculosis naturally lives and reproduces. The organism is spread
primarily as an airborne aerosol from an individual in the infectious stage of the disease, although transdermal and
gastrointestinal (GI) transmission is also possible.
DISEASE CONDITION: Active Tuberculosis

Active tuberculosis is a multiorgan disease caused by primary infection or as a reactivation


of latent tuberculosis. In human, a TB index case may infect a contact person through cough
and expectoration, so the lung is the primary route of infection and often the main tissue
exhibiting TB.

Infectious droplet nuclei are deposited in the alveolar spaces of the contact person where
Mycobacterium tuberculosis (M. tb) can be phagocytosed by alveolar macrophages,
epithelial cells, dendritic cells (DC) and neutrophils. Primary tuberculosis occurs when the
immune system is unable to defend against the Mycobacterium tuberculosis bacterium
(MTB) infection.

Thus, the bacteria multiply in the body, causing noticeable symptoms and rapid effects.
Though the lung is the most commonly involved organ, other organ systems may be
affected which includes the gastrointestinal system, the musculoskeletal system, the
lymphoreticular system, skin, liver, and the reproductive system.
DISEASE CONDITION: Active Tuberculosis

Infection to other people varies but most likely it is a shared contaminated air with a TB
positive person; talking, coughs, sneezes or speaking.
active TB patient’s breaths bacteria out into the air and anyone can acquire and be
infected/corrupted by them. Presumably spread it to their own household, workplace and
can definitely spread elsewhere.
CLASSIFICATION
Data from the history, physical examination, TB test, chest x-ray, and microbiologic studies are used to
classify TB into one of five classes.
• Class 0. There is no exposure or no infection.
• Class 1. There is an exposure but no evidence of infection.
• Class 2. There is latent infection but no disease.
• Class 3. There is a disease and is clinically active.
• Class 4. There is a disease but not clinically active.
• Class 5. There is a suspected disease but the diagnosis is pending.
CAUSES OF PTB
Causes of acquiring tuberculosis include the following:

• Close contact. Having close contact with someone who


has an active TB.
• Low immunity. Immunocompromised status like those
with HIV, cancer, or transplanted organs increases the risk
of acquiring tuberculosis.
• Substance abuse. People who are IV/injection drug users
and alcoholics have a greater chance of acquiring
tuberculosis.
• Inadequate health care. Any person without adequate
health care like the homeless, impoverished, and the
minorities often develop active TB.
• Immigration. Immigration from countries with a high
prevalence of TB could affect the patient.
• Overcrowding. Living in an overcrowded, substandard
housing increases the spreading of the infection.
Predisposing Factors:
Age: Children below 14
PATHOPHYSIOLOGY Precipitating Factors:

Immunocompromised person
y.o. and Adults more than Inhalation of droplet Malnourished Individuals
65 y.o. Economically-disadvantaged
infected with
Living in crowded areas
Native Americans, Mycobacterium
Alcohol abuse
Eskimos, Asians, and Tuberculosis Poor hygiene
people with color Lack of access to health care

It is trapped first in the When the initial prevention of


The bacteria is quickly
upper airways, where the infection is not successful, the
surrounded by
primary defenses is bacteria reaches and deposits
polymorphonuclear
activated referring to the itself in the lung periphery usually
leukocytes and engulfed by
mucus secreting goblet in the lower part of the upper lobe
the alveolar macrophages.
cell and the cilia. or the upper part of the lower
lobe; specifically in the alveoli.
Some mycobacterial organisms are carried
off by the lymphatics to the hilar lymph
nodes

It is now called the Gresultshon As a result of


As macrophages engulf the
Complex, but it rarely in the hypersensitivity to the
bacteria, these cells join and
spread to other body organs. organism, inside the giant
form into giant cells that encircle
cells caseous necrosis
the foreign cell.
occurs.

Collagenous scar tissue Fibrosis and calcification There is then the proliferation
encapsulates the tubercle to happens as the lesion ages of T-lymphocytes in the
separate the organisms from resulting to granuloma surrounding of the central core
the body. formation called as tubercle. of the caseous necrosis causing
some lesions.
As the process progress the bacteria may or
may not be killed and it continue to grow PULMONARY TUBERCULOSIS
and multiply resulting to a cell mediated
immunity
( which can be detected through PPD)

For poorly
The semiliquid necrotic material is
If drained in the bronchus immunocompromised clients,
drained into the bronchus or in the
as purulent discharge, it the necrotic tissue liquefies and
nearby blood vessel, leaving an air
could infect other people the fibrous walls losses its
filled cavity at the original site.
through droplet structural integrity
transmission.

EXTRAPULMONARY TUBERCULOSIS
Risk factorcs of active tuberculosis:

• History of HIV infection - Degree of


immunosuppression influence the clinical
manifestations.
• History of prior tuberculosis treatment
• History of a positive purified protein derivative
of the tuberculin test result
• Emigration from or travel to an area where
tuberculosis is endemic
• Contact with a person who has active TB
CLINICAL MANIFESTATIONS
After an incubation period of 4 to 8 weeks, TB is usually
asymptomatic in primary infection.

 Nonspecific symptoms. Nonspecific symptoms may be


produced such as fatigue, weakness, anorexia, weight loss,
night sweats, and low-grade fever, with fever and night
sweats as the typical hallmarks of tuberculosis.
 Cough. The patient may experience cough with
mucopurulent sputum.
 Hemoptysis. Occasional hemoptysis or blood on the
saliva is common in TB patients.
 Chest pains. The patient may also complain of chest pain
 as a part of discomfort.
COMPLICATIONS
If left untreated or mistreated, pulmonary tuberculosis may lead to:
• Respiratory failure. Respiratory failure is one of the most common complication of pulmonary
tuberculosis.
• Pneumothorax. Pneumothorax becomes a complication when tuberculosis is not treated properly.
• Pneumonia. One of the most fatal complications of tuberculosis is pneumonia as it could cause
infection all over the lungs.
• Without treatment, tuberculosis can be fatal. Untreated active disease typically affects your lungs, but it
can affect other parts of your body, as well.

Tuberculosis complications include:


• Spinal pain. Back pain and stiffness are common complications of tuberculosis.
• Joint damage. Arthritis that results from tuberculosis (tuberculous arthritis) usually affects the hips and
knees.
• Swelling of the membranes that cover your brain (meningitis). This can cause a lasting or
intermittent headache that occurs for weeks and possible mental changes.
• Liver or kidney problems. Your liver and kidneys help filter waste and impurities from your
bloodstream. Tuberculosis in these organs can impair their functions.
• Heart disorders. Rarely, tuberculosis can infect the tissues that surround your heart, causing
inflammation and fluid collections that might interfere with your heart's ability to pump effectively.
This condition, called cardiac tamponade, can be fatal.
Test to diagnose Active TB

Acid-fast bacilli (AFB) testing can be used to identify and confirm active


infection with M. tuberculosis as well as other Mycobacterium species.
(Mycobacteria are called acid-fast bacilli because they are rod-shaped
bacteria (bacilli) that can be seen under the microscope following a staining
procedure in which the bacteria retain the color of the stain after an acid
wash (acid-fast).) One or more of these tests may be performed when a
person has signs and symptoms or TB disease or screened positive for TB
infection.
 AFB smear — a microscopic examination of a specimen that has been stained to detect acid-fast bacteria, such as M.
tuberculosis. This test can provide probable (presumptive) results within a few hours. It is a valuable tool in helping
make decisions about treatment while culture results are pending.
 Molecular tests for TB (nucleic acid amplification test, NAAT) — detect the genetic components of TB bacteria in
a sputum sample and are often done when the AFB smear is positive or TB is highly suspected. Like AFB smears,
NAATs can provide a presumptive diagnosis, which can aid in the decision of whether to begin treatment before
culture results are available. Results of NAAT are typically available several hours after a sample is collected. One
type of NAAT detects within two hours the presence of M. tuberculosis and determines if it is resistant to rifampin, one
of the most commonly prescribed drugs used to treat TB. However, NAAT testing does not replace AFB cultures. All
samples submitted for AFB testing should be cultured to ensure that any mycobacteria that are present are available for
further testing, according to the Centers for Disease Control and Prevention.
 AFB cultures to grow the bacteria are set up at the same time as the AFB smears. Though more sensitive than AFB
smears, results of cultures may take days to several weeks.
 Susceptibility testing on the acid-fast bacteria grown in the cultures that are positive will determine the bacteria’s
susceptibility or resistance to drugs most commonly used to treat TB. Depending on the method used, results may be
available in 7 days or can take several weeks. There are molecular tests available that can also be used to detect
specific genes in the DNA of the bacteria that confer resistance to certain drugs.
 Sputum culture: Positive for Mycobacterium tuberculosis in the active stage of the disease.
 Ziehl-Neelsen (acid-fast stain applied to a smear of body fluid): Positive for acid-fast bacilli (AFB).
 Skin tests (purified protein derivative [PPD] or Old tuberculin [OT] administered by intradermal
injection [Mantoux]): A positive reaction (area of induration 10 mm or greater, occurring 48–72 hr
after interdermal injection of the antigen) indicates past infection and the presence of antibodies but is
not necessarily indicative of active disease. Factors associated with a decreased response to tuberculin
include underlying viral or bacterial infection, malnutrition, lymphadenopathy, overwhelming TB
infection, insufficient antigen injection, and conscious or unconscious bias. A significant reaction in a
patient who is clinically ill means that active TB cannot be dismissed as a diagnostic possibility. A
significant reaction in healthy persons usually signifies dormant TB or an infection caused by a
different mycobacterium.
 Enzyme-linked immunosorbent assay (ELISA)/Western blot: May reveal presence of HIV.
 Chest x-ray: May show small, patchy infiltrations of early lesions in the upper-lung field, calcium
deposits of healed primary lesions, or fluid of an effusion. Changes indicating more advanced TB may
include cavitation, scar tissue/fibrotic areas.
 CT or MRI scan: Determines degree of lung damage and may confirm a difficult diagnosis.
 Histologic or tissue cultures (including gastric washings; urine and cerebrospinal fluid [CSF];
skin biopsy): Positive for Myco­bacterium tuberculosis and may indicate extrapulmonary
involvement.
 Needle biopsy of lung tissue: Positive for granulomas of TB; presence of giant cells indicating
necrosis.
 Electrolytes: May be abnormal depending on the location and severity of infection; e.g., 
hyponatremia caused by abnormal water retention may be found in extensive chronic pulmonary
TB.
 ABGs: May be abnormal depending on location, severity, and residual damage to the lungs.
 Pulmonary function studies: Decreased vital capacity, increased dead space, increased ratio of
residual air to total lung capacity, and decreased oxygen saturation are secondary to parenchymal
infiltration/fibrosis, loss of lung tissue, and pleural disease (extensive chronic pulmonary TB).
MEDICAL
MANAGEMENT
Pharmacologic Theraphy
The first line antituberculosis medications include:

 Isoniazid (INH). INH is a bactericidal agent that is used as prophylaxis for neuritis, and has side effects of peripheral
neuritis, hepatic enzyme elevation, hepatitis, and hypersensitivity.
 Rifampin (Rifadin). Rifampin is a bactericidal agent that turns the urine and other body secretions into orange or red,
and has common side effects of hepatitis, febrile reaction, purpura, nausea, and vomiting.
 Pyrazinamide. Pyrazinamide is a bactericidal agent which increases the uric acid in the blood and has common side
effects of hyperuricemia, hepatotoxicity, skin rash, arthralgias, and GI distress.
 Ethambutol (Myambutol). Ethambutol is a bacteriostatic agent that should be used with caution with renal disease, and
has common side effects of optic neuritis and skin rash.
 Second-line drugs: ethionamide (Trecator-SC), para-aminosalicylate (PAS), cycloserine (Seromycin), capreomycin
(Capastat).
 
 If drug-resistant TB, report to physician, might give one or more different medicines. may have to take them for much
longer, up to 30 months, and they can cause more side effects.
Pulmonary tuberculosis is treated primarily with antituberculosis agents for 6 to 12 months.

• First line treatment. First-line agents for the treatment of tuberculosis are isoniazid (INH),
rifampin (RIF), ethambutol (EMB), and pyrazinamide.
• Active TB. For most adults with active TB, the recommended dosing includes the administration
of all four drugs daily for 2 months, followed by 4 months of INH and RIF.
• Initial phase. The initial phase consists of a multiple-medication regimen of INH, rifampin,
pyrazinamide, and ethambutol and lasts for 8 weeks.
• Continuation phase. The continuation phase of treatment include INH and rifampin or INH and
rifapentine, and lasts for an additional 4 or 7 months.
• Prophylactic isoniazid. Prophylactic INH treatment involves taking daily doses for 6 to 12
months.
• DOT. Directly observed therapy may be selected, wherein an assigned caregiver directly observes
the administration of the drug. an additional treatment regimen is undergone by patients called
directly observed therapy short-term (DOTS), which closely monitors treatment adherence and
completion [6], with the goal of efficiency and cost-effectiveness [1]. With the emergence of
MDR-TB, DOTS-plus was initiated as a more rigorous treatment strategy

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