FOREWORD

Praise and gratitude to Allah, who has bestowed His grace so that the author
can finish writing this paper, to complete the requirements of the Senior Clinic
Partnership of the SMF Mental Health Sciences General Hospital Dr. Pirngadi
Medan with the title "Tuberculosis". On this occasion, the authors would like to
thank the SMF Lung Sciences, especially the author's supervisor and all teaching
staff at the SMF Lung General Hospital Dr. Pirngadi Medan, as well as friends at
the Senior Clinic Partnership.
The author realizes that this paper has many shortcomings both from the
completeness of the theory and the language spoken. Therefore, the authors expect
criticism and constructive suggestions for the perfection of this paper. The author
hopes that this paper can benefit us all.

Medan, 01 September 2019

Author

i
 TABLE OF CONTENTS

FOREWORD ........................................................................................................ i

TABLE OF CONTENTS ..................................................................................... ii

CHAPTER 1 Tuberculosis ................................................................................... 1

CHAPTER 2 THE BASIC SCIENCE .................................................................4

2.1 Definition .............................................................................................. 4

2.2 Epidemiology ........................................................................................4

2.3 Etiology ..................................................................................................6

2.4 Pathogenesis ...........................................................................................7

2.5 Risk Factors ............................................................................................9

2.6 Signs and Symptoms ..............................................................................9

2.7 Diagnosis ..............................................................................................12

2.8 TB Treatment Regimens ......................................................................15

2.9 Prognosis…..........................................................................................16

CHAPTER 3 CONCLUSION .............................................................................17

REFERENCES ....................................................................................................21

ii
 CHAPTER 1
Tuberculosis

Despite the availability of a cheap and effective treatment, tuberculosis still

accounts for millions of cases of active disease and deaths worldwide. The disease
disproportionately affects the poorest persons in both high-income and developing
countries.1 However, recent advances in diagnostics, drugs, and vaccines and
enhanced implementation of existing interventions have increased the prospects for
improved clinical care and global tuberculosis control.1
It is with great pleasure that we announce the launch of a new journal
dedicated to tuberculosis and other mycobacterial diseases.Tuberculosis (TB)
remains a major global health problem. In 2013,an estimated 9.0 million people
developed TB and 1.5 million died from the disease. Tuberculosis is the second
leading cause of death from an infectious disease worldwide, after the human
immunodeficiency virus infection. While there has been progress in the efforts to
control tuberculosis, considerable work remains to be done to achieve the
Millennium Development Goals of reducing the global burden of tuberculosis.
There has been a resurgence of interest among scientists and commercial companies
in investigating how tuberculosis causes disease and acquires resistance to drugs;
there is interest in developing new diagnostic methods, vaccines, and therapeutics
as well.More than 50 companies are involved in development of new diagnostic
tests. At least 10 new or repurposed TB drugs are in late phases of clinical
development. There are 10 vaccines for TB prevention and 2 immunotherapeutic
vaccines in the pipeline.1
Determining the global burden of non-tuberculous (NTM) mycobacterial
infections is difficult because reporting these infections to public health
departments is not required. Nevertheless, published reports indicate that non-
tuberculous mycobacterial infections are increasing. The treatment of these
infections is more problematic than many people realize. Many NTM organisms
are resistant to currently available antibiotics and require a longer course of

1
treatment than tuberculosis. The cost associated with managing these infections
may be several fold than that of tuberculosis.2,3

Throughout history, the tropics (Indonesia) have been more easily

infected infectious diseases compared to temperate regions infection. The main
reason is due to environmental factors with humidity quite high, so that all living
things grow well, including pathogens, vectors, and hosts. This is compounded by
our awareness factor to try to control infectious diseases or tropical diseases
comprehensively-systematically still lacking. One example of a disease tropical is
tuberculosis and as the main cause of death as global infectious disease. This case
increases, if there is an interaction between TB and HIV epidemic. In many regions
of the world specifically in Our country, this disease attacks people of all ages and
is aggravated with the increase in resistance of pathogenic bacteria to synthetic
drugs. Treatment of TB caused by M. tuberculosis still sensitive Sensitive-
Tuberculosis Drug (DS-TB) requires Drug combinations consisting of 4-5 types of
drugs for 6 months or more.Standard therapy for DS-TB patients including a
combination of isoniazid, rifampicin, pyrazinamide and ethambutol for the first 2
months and isoniazid combination and rifampicin alone for the next 4 months.1,2

In 2011, there were 8.7 million new cases of active tuberculosis worldwide
(13% of which involved coinfection with the human immunodeficiency virus
[HIV]) and 1.4 million deaths, including 430,000 deaths among HIV-infected
patients1 representing a slight decrease from peak numbers in the mid-2000s (Fig.
1). It has been estimated that there were 310,000 incident cases of multidrug-
resistant tuberculosis, caused by organisms resistant to at least isoniazid and
rifampin, among patients who were reported to have tuberculosis in 2011 (Fig. 2).
More than 60% of these patients were in China, India, the Russian Federation,
Pakistan, and South Africa.1,2 A total of 84 countries have reported cases of
extensively drug-resistant tuberculosis, a subset of multidrug-resistant tuberculosis
with added resistance to all fluoroquinolones plus any of the three injectable
antituberculosis drugs, kanamycin, amikacin, and capreomycin.1-3 Sub-Saharan

2
Africa has the highest rates of active tuberculosis per capita, driven primarily by
the HIV epidemic.1 The absolute number of cases is highest in Asia, with India and
China having the greatest burden of disease globally.1 In the United States and most
Western European countries, the majority of cases occur in foreign-born residents
and recent immigrants from countries in which tuberculosis is endemic.4-6
Patients with active pulmonary tuberculosis are the source of
Mycobacterium tuberculosis. In more than 90% of persons infected with M.
tuberculosis, the pathogen is contained as asymptomatic latent infection. Recent
studies raise the possibility that some persons acquire and eliminate acute infection
with M. tuberculosis. 7 The risk of active disease is estimated to be approximately
5% in the 18 months after initial infection and then approximately 5% for the
remaining lifetime.8 An estimated 2 billion persons worldwide have latent infection
and are at risk for reactivation.1 Contained latent infection reduces the risk of
reinfection on repeated exposure, whereas active tuberculosis is associated with an
increased risk of a second episode of tuberculosis on reexposure (Fig. S1 in the
Supplementary Appendix, available with the full text of this article at
NEJM.org).8,9,10

3
 CHAPTER 2

THE BASIC SCIENCE OF TUBERCULOSIS

2.1 Definition

Tuberculosis is a bacterial disease spread from one person to another

principally by airborne transmission. The causal agent is Mycobacterium
tuberculosis (the tubercle bacillus). In a small proportion of cases, the bacillus is
transmitted to humans from infected cows through drinking non-sterilized milk.
This mode of transmission plays only a minor role in the natural history of the
disease in humans. Tuberculosis can affect any organ in the body. Pulmonary
tuberculosis is the most frequent site of involvement; extrapulmonary tuberculosis
is less frequent. Only pulmonary tuberculosis is infectious1,2

2.2 Epidemiology

In 2011, there were 8.7 million new cases of active tuberculosis worldwide
(13% of which involved coinfection with the human immunodeficiency virus
[HIV]) and 1.4 million deaths, including 430,000 deaths among HIV-infected
patients1 representing a slight decrease from peak numbers in the mid-2000s (Fig.
1). It has been estimated that there were 310,000 incident cases of multidrug-
resistant tuberculosis, caused by organisms resistant to at least isoniazid and
rifampin, among patients who were reported to have tuberculosis in 2011 (Fig.
2).1,2,3More than 60% of these patients were in China, India, the Russian Federation,
Pakistan, and South Africa.1,2 A total of 84 countries have reported cases of
extensively drug-resistant tuberculosis, a subset of multidrug-resistant tuberculosis
with added resistance to all fluoroquinolones plus any of the three injectable
antituberculosis drugs, kanamycin, amikacin, and capreomycin.1-3 Sub-Saharan
Africa has the highest rates of active tuberculosis per capita, driven primarily by
the HIV epidemic.1 The absolute number of cases is highest in Asia, with India and
China having the greatest burden of disease globally.1 In the United States and most
Western European countries, the majority of cases occur in foreign-born residents
and recent immigrants from countries in which tuberculosis is endemic May have

4
evolved from M bovis; acquired by humans from domesticated animals ~15,000
years ago.Endemic in humans when stable networks of 200-440 people established
(villages) ~ 10,000 years ago; Epidemic in Europe after 1600 (cities). 354-322 BC
- Aristotle – “When one comes near consumptives one does contract their
disease.The reason is that the breath is bad and heavy In approaching the
consumptive, one breathes this pernicious air. One takes the disease because in this
air there is something disease producing.4,5,6

5
2.3 Etiology

Mycobacterium tuberculosis is a causative bacteriatuberculosis. M.

tuberculosis and seven other very speciesclose to mycobacteria (M. bovis, M.
africanum, M. microti, M.caprae, M. pinnipedii, M. canetti and M. mungi) together
forming the M. tuberculosis complex. Not all species cause disease in humans. The
majority of TB cases in United States caused by M. tuberculosis. M. tuberculosis is
also called as tubercle Bacilli. Mycobacterium bovis (M. bovis) is another type of
mycobacteria as a cause of TB in human. M.bovis is most commonly found in
cattle, bison, and deer Mycobacteria represent a very old genus of bacteria because
it has been on earth for millions of years and has been adapt to almost all
environments on earth such as water, land, dust and air. Various evidence from the
results of research on the tomb mummies in Egypt are available to support this
statement. Mycobacteria goes inside the Mycobacteriaceae family and the
Actinomycetales order. Genus Mycobacteria have close relationships with
members 12 Other Actinomycetales such as Corynebacterium, Nocardia and
Rhodococcus.5,7,11 The following is a classification of mycobacteria
Kingdom: Bacteria
Phylum: Actinobacteria
Order: Actinomycetales
Suborder: Corynebacterineae
Family: Mycobacteriaceae
Genus: Mycobacterium
In general, the color and morphology of mycobacteria are growing in solid
culture media is the main marker of this microorganism. Most species are whitish
or white colonies,but especially in species that have their rapid growth is bright
yellow or orange species because of the carotenoid pigment content.The type of
color and the ability of strains to produce color in darkness (scotochromogenic
species) or in response against light (photochromogenic species) used as method
for classification of potentially pathogenic mycobacteria.7,8

6
 The main reservoir of M. tuberculosis is the patient with pulmonary
tuberculosis. Such patients may have pulmonary “cavities” that are rich in bacilli
(100 million bacilli in a cavity of approximately 2cm in diameter). The diagnosis
of pulmonary tuberculosis is straightforward in such patients, as they almost always
have chronic respiratory symptoms such as cough and sputum production. The
definitive diagnosis is simple when the patient has large numbers of bacilli in the
sputum (more than 5000 bacilli/ml), as these can be seen on microscopic
examination of a sputum smear; these patients are termed “smear-positive”.7

2.4 Pathogenesis16

Infection occurs when a person inhales droplet nuclei containing tubercle

bacilli that reach the alveoli of the lungs. These tubercle bacilli are ingested by
alveolar macrophages; the majority of these bacilli are destroyed or inhibited. A
small number may multiply intracellularly and are released when the macrophages
die. If alive, these bacilli may spread by way of lymphatic channels or through the
bloodstream to more distant tissues and organs (including areas of the body in

which TB disease
 is most likely to develop: regional lymph nodes, apex of the

lung, kidneys, brain, and bone). This process of dissemination primes the immune
system for a systemic response.

Droplet nuclei containing tubercle bacilli

are inhaled, enter the lungs, and travel to
the alveoli.

7
 Tubercle bacilli multiply in
the alveoli.

A small number of tubercle

bacilli enter the bloodstream
and spread throughout the
body. the tubercle bacilli may
reach any part of the body,
including areas where TB
disease is more likely to
develop (such as the brain,
larynx, lymph node, lung,
spine, bone, or kidney.

8
Within 2 to 8 weeks, special
immune cells called
macrophages ingest and
surround the tubercle bacilli.
The cells form a barrier shell,
called a granuloma, that
keeps the bacilli contained
and under control.

The immune system cannot

keep the tubercle bacilli
under control, the bacilli
begin to multiply rapidly (TB
disease). This process can
occur in different areas in the
body, such as the lungs,
kidneys, brain, or bone.

9
2.5 Risk Factors for TB Disease15

 Low socioeconomic status

 Homelessness
 Diseases, conditions or drgs that weaken the immune system
 Cancer
 Transplantation
 Malnutrition
 Diabetes
 Alcoholism
 HIV infection
 TB is the leading cause of death worldwide in HIV infected
individuals
 10% lifetime risk for developing active TB among HIV
uninfected
 10% annual risk for developing active TB among HIV
infected
• Major surgical procedures may occasionally trigger dissemination

2.6 Signs and Symptoms of TB Disease12,17

The classic clinical features of pulmonary tuberculosis include chronic

cough, sputum production, appetite loss, weight loss, fever, night sweats, and
hemoptysis.17 Extrapulmonary tuberculosis occurs in 10 to 42% of patients,
depending on race or ethnic background, age, presence or absence of underlying
disease, genotype of the M. tuberculosis strain, and immune status.18
Extrapulmonary tuberculosis can affect any organ in the body, has varied and
protean clinical manifestations, and therefore requires a high index of clinical
suspicion. HIV coinfection poses special challenges to clinical management in
patients with active tuberculosis. The risk of active tuberculosis increases soon after
infection with HIV19 and the manifestations of pulmonary tuberculosis at this stage
are similar to those in HIV-negative persons. At CD4 counts of less than 200 per

10
cubic millimeter, the presentation of tuberculosis may be atypical, with subtle
infiltrates, pleural effusions, hilar lymphadenopathy, and other forms of
extrapulmonary tuberculosis in as many as 50% of patients. At CD4 counts of less
than 75 per cubic millimeter, pulmonary findings may be absent, and disseminated
tuberculosis, manifested as a nonspecific, chronic febrile illness with widespread
organ involvement and mycobacteremia, is more frequent, with high early
mortality; polyclonal disease has also been described.20 Such cases may be
mistakenly diagnosed as other infectious diseases and are often identified only on
autopsy.14

Asymptomatic, subclinical tuberculosis, with negative findings on a sputum

smear and chest radiography and positive culture results, is a common feature of
HIV-associated tuberculosis and may account for 10% of cases in regions in which
tuberculosis is endemic.13,17,19 Up to 25% of patients presenting for HIV care in
such regions have undiagnosed active tuberculosis.1 Therefore, screening for
tuberculosis is recommended for all patients with HIV infection to identify patients
with active disease and before 0–299 300–2999 3000–29,999 30,000–59,999
≥60,000 Data not shown MDR-TB Global Numbers of Cases of Multidrug-
Resistant Tuberculosis. Shown are the estimated numbers of cases of multidrug-
resistant disease (including extensively drug-resistant disease) among cases of
pulmonary tuberculosis that were officially reported in 2011. The presence of any
one of four symptoms (cough, fever, night sweats, or weight loss) has been shown
to have sensitivity in the range of 80% for identifying patients in whom further
diagnostic evaluation is warranted, even in resource-constrained regions.20

Proactive screening for tuberculosis is recommended in areas where the

disease is highly endemic, since subclinical tuberculosis in patients with HIV
infection or noncommunicable diseases (e.g., diabetes mellitus and tobacco-related
chronic lung disease) may otherwise be missed.11

 Extrapulmonary TB
 M. tuberculosis can infect any organ of the body

11
  Symptoms vary by site of disease
 Pulmonary TB
 Cough >2 weeks
 often productive (sputum) can be bloody
 Fever
 Night sweats
 Weight loss
 Chest pain

2.7 Diagnosis of TB Disease 10

 Latent Infection
Screening and treatment for latent M. tuberculosis infection are indicated
for groups in which the prevalence of latent infection is high (e.g., foreignborn
persons from regions in which tuberculosis is endemic), those in whom the risk of
reactivated disease is high (e.g., patients with HIV infection or diabetes and patients
receiving immunosuppressive therapy), and those with both factors (e.g., recent
contacts of patients with tuberculosis). Latent infection can be diagnosed with either
a tuberculin skin test or an interferon-gamma release assay. Specific guidelines
from the Centers for Disease Control and Prevention in the United States, the
National Institute for Health and Clinical Excellence in the United Kingdom, and
the European Centre for Disease Prevention and Control30 recommend the use of
the interferon-gamma release assay and tuberculin skin test for screening for latent
M. tuberculosis infection in various age and risk groups. The tuberculin skin test is
less expensive and is therefore preferred in low-income regions. It is as sensitive as
the interferon-gamma release assay but less specific.

 Active Tuberculosis
Sputum microscopy and culture in liquid medium with subsequent drug-
susceptibility testing are currently recommended as standard methods for
diagnosing active tuberculosis. The use of solid culture medium is more cost-
effective in resourcepoor countries. Interferon-gamma release assays and tuberculin

12
skin tests have no role in the diagnosis of active disease.Nucleic acid amplification
tests, imaging, and histopathological examination of biopsy samples supplement
these evaluations. In resource-constrained settings with a high prevalence of
tuberculosis and HIV infection, an estimated 30% of all patients with tuberculosis
and more than 90% of those with multidrug-resistant and extensively drug-resistant
tuberculosis do not receive a diagnosis.1-3 A new molecular diagnostic test called
Xpert MTB/RIF assay detects M. tuberculosis complex within 2 hours, with an
assay sensitivity that is much higher than that of smear microscopy.34 In
HIVinfected patients, the test has a rate of case detection that is increased by 45%,
as compared with smear microscopy. This molecular assay has the potential to
improve the performance of national tuberculosis programs and is currently being
implemented in district-level laboratories in 67 countries with a high prevalence of
tuberculosis.1 It is available in Europe and is being examined for approval in the
United States.10
 Drug-Resistant Tuberculosis
The current standard for first-line drug-susceptibility testing is an automated
liquid culture system, which requires 4 to 13 days for results. Commercial
molecular line-probe assays can yield results in 24 hours, once they have been
validated against automated liquid culture. Within 2 hours, the Xpert MTB/RIF
assay concurrently gives results on rifampin resistance, a proxy of multidrug-
resistant tuberculosis in settings in which there is a high prevalence of drug
resistance, since rifampin resistance in the absence of isoniazid resistance is
uncommon. Assay modifications have been introduced to reduce false positive
results with respect to rifampin resistance. The World Health Organization (WHO)
recommends that standard drug-susceptibility testing be performed at the same time
that the Xpert MTB/RIF assay is performed to confirm rifampin resistance and the
susceptibility of the M. tuberculosis isolate to other drugs. Other screening tests for
drug resistance include the microscopic-observation drug-susceptibility (MODS)
assay, the nitrate reductase assay, and colorimetric reductase methods. The MODS
assay simultaneously detects M. tuberculosis bacilli, on the basis of cording
formation, and isoniazid and rifampin resistance.Since most of these methods are

13
not currently available in countries in which tuberculosis is highly endemic, it is
estimated that only 10% of cases of multidrug-resistant tuberculosis are currently
diagnosed worldwide and only half of them receive appropriate treatment.10

Signs and Symptoms consistent with TB 16

• Chest X-ray
• Clinical Judgment
• Bacteriology
– AFB smear microscopy
– Nucleic Acid Amplification Testing (NAAT)
– Culture and Identification
– Drug susceptibility testing (DST)

 Tuberculin skin test

Tuberculin is prepared from metabolic products of M. tuberculosis bacilli,
and therefore contains a number of polyantigenic proteins. In infected subjects,
intradermal injection of tuberculin provokes the liberation of lymphokines that
cause a delayed-type hypersensitivity reaction, demonstrated by the appearance 24–
72 hours later of a localized infiltration of inflammatory cells into the skin, causing
a swelling at the site of injection. 10
The delayed-type hypersensitivity reaction induced by microbial antigens
of M. tuberculosis is also induced by BCG bacilli, and by certain environmental
mycobacteria.
The tuberculin skin test reaction is used:
- In individuals, to diagnose tuberculous infection. A significant reaction
indicates that the subject has been infected by mycobacteria at some stage.
It does not provide proof of tuberculosis disease.
- In the community, surveys using the tuberculin skin test in a representative
sample of non-BCG-vaccinated children determine the proportion of
infected subjects in the sample. This proportion provides an indication of

14
 the rate of infection in this community, from which the annual risk of
tuberculosis infection (ARI) can be calculated.10
 Serological tests for tuberculosis10
Serological tests attempt to demonstrate the presence of circulating
antibodies, using mycobacterial antigens. The recognition of antigens by the
antibodies present in infected individuals could aid in the diagnosis of disease at
certain extrapulmonary sites for which diagnosis by bacteriology or histology is
difficult. However, these costly tests are not yet sufficiently sensitive or specific to
be of routine practical use.

2.8 TB Treatment Regimens15,16,20

 TB Infection – LTBI treatment options

o 9 months isoniazid
o 4 months rifampin
o 3 months isoniazid plus rifapentine
 TB Disease – pulmonary, drug susceptible TB, 6- month standard regimen
o Intensive phase: 2 months isoniazid, rifampin, ethambutol, and
pyrazinamide
o Continuation phase: 4 months of isoniazid and rifampin
 Drug Resistant TB
o Multidrug resistant TB (MDR TB)—resistant to at least rifampin
(RIF) and isoniazid (INH)
o 3.7% of new cases worldwide are estimated to have MDR TB (20%
among previously treated TB cases)
o 50% of all MDR cases are estimated to occur in India and China
o Globally, outcome data for MDR TB is limited. Highest death rates
among MDR TB patients seen in African region (19%)
o Extensively drug resistant TB (XDR TB)—MDR TB plus resistance
to at least 1 fluoroquinolone and 1 second-line injectable drug15,16,20
 MDR TB Treatment

15
 o 2 years of therapy with second-line drugs
o Expensive and drugs may not be readily available
o Second-line drugs often cause severe adverse effects and are very
difficult for patients to tolerate
o Increasing resistance to second-line drugs due to frequent changes
in regimens (often due to toxicity), poor adherence, too few effective
drugs available for regimen15,16,20

2.9 Prognosis 20

A number of studies have shown that over a period of 5 to 10 years after

hospitalization for pulmonary patients, only about 80% of patients can be described
as having good outcomes (ad Bonam). More than 20% of patients can be described
as having poor outcomes. (dubia ad Bonam).
Quo ad Vitam : ad bonam

Quo ad functionam : dubia ad bonam

Quo ad Sanationam : ad bonam

16
 CHAPTER 3

CONCLUSION

Despite the availability of a cheap and effective treatment, tuberculosis still

accounts for millions of cases of active disease and deaths worldwide. The disease
disproportionately affects the poorest persons in both high-income and developing
countries.1 However, recent advances in diagnostics, drugs, and vaccines and
enhanced implementation of existing interventions have increased the prospects for
improved clinical care and global tuberculosis control.1
Tuberculosis is a bacterial disease spread from one person to another
principally by airborne transmission. The causal agent is Mycobacterium
tuberculosis (the tubercle bacillus). In a small proportion of cases, the bacillus is
transmitted to humans from infected cows through drinking non-sterilized milk.
This mode of transmission plays only a minor role in the natural history of the
disease in humans. Tuberculosis can affect any organ in the body. Pulmonary
tuberculosis is the most frequent site of involvement; extrapulmonary tuberculosis
is less frequent. Only pulmonary tuberculosis is infectious1,2
In 2011, there were 8.7 million new cases of active tuberculosis worldwide
(13% of which involved coinfection with the human immunodeficiency virus
[HIV]) and 1.4 million deaths, including 430,000 deaths among HIV-infected
patients1 representing a slight decrease from peak numbers in the mid-2000s (Fig.
1). It has been estimated that there were 310,000 incident cases of multidrug-
resistant tuberculosis, caused by organisms resistant to at least isoniazid and
rifampin, among patients who were reported to have tuberculosis in 2011 (Fig.
2).1,2,3More than 60% of these patients were in China, India, the Russian Federation,
Pakistan, and South Africa.1,2 A total of 84 countries have reported cases of
extensively drug-resistant tuberculosis, a subset of multidrug-resistant tuberculosis
with added resistance to all fluoroquinolones plus any of the three injectable
antituberculosis drugs, kanamycin, amikacin, and capreomycin.1-3 Sub-Saharan

17
Africa has the highest rates of active tuberculosis per capita, driven primarily by
the HIV epidemic.
Mycobacterium tuberculosis is a causative bacteriatuberculosis. M.
tuberculosis and seven other very speciesclose to mycobacteria (M. bovis, M.
africanum, M. microti, M.caprae, M. pinnipedii, M. canetti and M. mungi) together
forming the M. tuberculosis complex. Not all species cause disease in humans. The
majority of TB cases in United States caused by M. tuberculosis. M. tuberculosis is
also called as tubercle Bacilli. Mycobacterium bovis (M. bovis) is another type of
mycobacteria as a cause of TB in human. M.bovis is most commonly found in
cattle, bison, and deer Mycobacteria represent a very old genus of bacteria because
it has been on earth for millions of years and has been adapt to almost all
environments on earth such as water, land, dust and air. Various evidence from the
results of research on the tomb mummies in Egypt are available to support this
statement. Mycobacteria goes inside the Mycobacteriaceae family and the
Actinomycetales order. Genus Mycobacteria have close relationships with
members 12 Other Actinomycetales such as Corynebacterium, Nocardia and
Rhodococcus.5,7,11 The following is a classification of mycobacteria
Kingdom: Bacteria
Phylum: Actinobacteria
Order: Actinomycetales
Suborder: Corynebacterineae
Family: Mycobacteriaceae
Genus: Mycobacterium
Patients with active pulmonary tuberculosis are the source of
Mycobacterium tuberculosis. In more than 90% of persons infected with M.
tuberculosis, the pathogen is contained as asymptomatic latent infection. Recent
studies raise the possibility that some persons acquire and eliminate acute infection
with M. tuberculosis. 7 The risk of active disease is estimated to be approximately
5% in the 18 months after initial infection and then approximately 5% for the
remaining lifetime.8 An estimated 2 billion persons worldwide have latent infection
and are at risk for reactivation.1 Contained latent infection reduces the risk of

18
reinfection on repeated exposure, whereas active tuberculosis is associated with an
increased risk of a second episode of tuberculosis on reexposure .8,9,10

 Signs and Symptoms consistent with TB 16

• Chest X-ray
• Clinical Judgment
• Bacteriology
– AFB smear microscopy
– Nucleic Acid Amplification Testing (NAAT)
– Culture and Identification
– Drug susceptibility testing (DST)
TB Treatment Regimens15,16,20

 TB Infection – LTBI treatment options

o 9 months isoniazid
o 4 months rifampin
o 3 months isoniazid plus rifapentine
 TB Disease – pulmonary, drug susceptible TB, 6- month standard regimen
o Intensive phase: 2 months isoniazid, rifampin, ethambutol, and
pyrazinamide
o Continuation phase: 4 months of isoniazid and rifampin
 Drug Resistant TB
o Multidrug resistant TB (MDR TB)—resistant to at least rifampin
(RIF) and isoniazid (INH)
o 3.7% of new cases worldwide are estimated to have MDR TB (20%
among previously treated TB cases)
o 50% of all MDR cases are estimated to occur in India and China
o Globally, outcome data for MDR TB is limited. Highest death rates
among MDR TB patients seen in African region (19%)
o Extensively drug resistant TB (XDR TB)—MDR TB plus resistance
to at least 1 fluoroquinolone and 1 second-line injectable drug15,16,20

19
  MDR TB Treatment
o 2 years of therapy with second-line drugs
o Expensive and drugs may not be readily available
o Second-line drugs often cause severe adverse effects and are very
difficult for patients to tolerate
o Increasing resistance to second-line drugs due to frequent changes
in regimens (often due to toxicity), poor adherence, too few effective
drugs available for regimen15,16,20
Prognosis

Quo ad Vitam : ad bonam

Quo ad functionam : dubia ad bonam

Quo ad Sanationam : ad bonam

20
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