Paper of Module V

INFECTIOUS DISEASE

C-1
(Name and NIM are attached on the next page)

FACULTY OF DENTAL MEDICINE

UNIVERSITAS AIRLANGGA
SURABAYA
2019
 MEMBER’S NAME:

Muhammad Arya Rizkianto 021711133110

Novita 021711133111
Cindy Shavia 021711133112
GempitaAnargia 021711133113
Farah MaulidyaTitani 021711133114
Titian Fauzi Nurrahman 021711133115
Faizal KhalisRamadhani 021711133116
Alifia Ummu Risya 021711133117
Putu Hiroko Anindya Putri Suardita 021711133118
Mohammad RaidjffanZulkarnaenTabona 021711133119
R. DevatharaArdhisatrya 021711133120
Seno Fauzi Alyanugraha 021711133121
Muhammad Zaydan 021711133122

2
 PREFACE

By mentioning the name of Allah SWT, the Most Gracious, the Most
Merciful. We offer worship and praise for the presence of Him, who has bestowed
His mercy, guidance, and blessings on us, so that we can complete this paper. We
have compiled this paper by getting help from various parties so that we would
like to express our gratitude to all those who have contributed to the making of
this paper. Apart from all that, we are fully aware that there are still shortcomings
in terms of both the composition of the sentence and the grammar. Therefore, we
accept all suggestions and criticisms from readers so that we can improve this
paper.
Finally, we hope that this paper can add to the readers' insight.

Surabaya, November 2019

Author

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 TABLE OF CONTENTS
COVER....................................................................................................................i

PREFACE.............................................................................................................iii

TABLE OF CONTENTS.......................................................................................4

INTRODUCTION..................................................................................................5

1.1. Background...............................................................................................5

1.2. Formulations of the problem.....................................................................5

1.3. Purpose of Writing....................................................................................5

1.4. Benefits......................................................................................................6

1.5. Issues.........................................................................................................6

CONTENT..............................................................................................................7

2.1. Infection.....................................................................................................7

2.2. Tuberculosis..............................................................................................9

2.2.1. Hematogenic TB Spread....................................................................9

2.2.2. Spread of TB in the lung..................................................................10

2.2.3. Pathogenesis of TBC........................................................................13

2.2.4. Clinical symptoms of TBC..............................................................14

2.2.5. TBC Examination............................................................................15

CONCEPTUAL MAPPING................................................................................18

DISCUSSION.......................................................................................................19

CONCLUSION.....................................................................................................21

5.1. Conclusion...............................................................................................21

BIBLIOGRAPHY................................................................................................22

4
 Chapter I

INTRODUCTION

1.1. Background
The oral cavity is one of the entry windows of a disease. Oral health can give
an idea of the level of general health of individuals. There are various kinds of
problems that can occur in the oral cavity, both originating from the oral cavity
itself and manifestations of systemic disease.
In the oral cavity can occur a lesion caused by manifestations of systemic
disease. Lesions are pathological disorders that cause symptoms. One of the
systemic diseases that manifests in the oral cavity in the form of thrush lesions is
Tuberculosis.
In the case given, the patient complained of thrush on the tongue for 1 month
and did not heal even though it had been treated. Thrush causes discomfort and
results in weight loss. After collecting the history data, the alleged cause of the
lesion is related to the tuberculosis disease suffered by the patient.
1.2. Formulations of the problem
What is the diagnosis and pathogenesis of patient’s disease?
1.3. Purpose of Writing
1. General Purpose
After completing this module, 5th semester students of the Faculty of
Dentistry, Airlangga University were able to explain the mechanism of
odontogenic and non-odontogenic infections, interactions of
microorganisms with hosts, reviewed from clinical, pathobiological,
pathological, immunological, microbiological, and x-ray aspects as well as
their relationship with systemic infectious diseases.
2. Special Purpose
After completing this module 5, 5th semester students of the Faculty
of Dental Medicine, Airlangga University were able to explain:
1) The basic concept of infection in general.
2) Local infection mechanism

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 3) The mechanism of systemic infection
4) The mechanism of spread of local infection into systemic or
systemic infection to the local oral cavity.
1.4. Benefits
1. Providing insight into the relationship between TB disease and stomatitis
to the public.
2. Provide information to the public that tuberculosis has clinical
manifestations in the oral cavity in the form of stomatitis.
1.5. Issues
A man came to the dentist's clinic complaining of stomatitis on the
tongue for 1 month. Although mouthwash had been administered, canker
sores has not healed. The presence of canker sores makes eating
uncomfortable and causes weight loss. After anamnesis and intra and extra
oral examination, the dentist refers the patient to an internist.

6
 Chapter II

CONTENT
2.1. Infection
Infection is a process of invasion and also multiplications of
microorganism (such as bacteria, virus, and parasite) which causes
pathological conditions. Infection can cause clinical symptoms and not. There
are two types of infection, local infection and systemic infection. Local
infection can spread through blood and lymph vessel and become systemic
infection.
The process experienced by bacteria before infection is colonization.
Colonization Is a process in which the seeds of microorganisms become
resident flora. Microorganisms can grow and multiply but cannot cause
disease. Infection occurs when the microorganisms that have settled
successfully invade / attack parts of the body / human host whose defense
system is ineffective and pathogens cause tissue damage. After bacteria
colonize specific local infections will occur and are limited to the part of the
body where microorganisms live. If local infections are not treated properly, a
systemic infection occurs where microorganisms spread to other parts of the
body and cause damage. All of these stages called chain of infection and
consist of:(Tyshenko MG, 2015).
1. Infectious agent
Types of microorganism which causes infection:
a. Virus d. Protozoa
b. Bacteria e. Parasite
c. Fungi

2. Reservoir
Reservoir is place for infection agent usually lives and multiplies, such as
animal, human and also environment.
a. Human Reservoir: patient with agent infection with clinical symptoms
and asymptomatic (carrier).
b. Animal reservoir: avian influenza, brucellosis, anthrax, etc.

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 c. Environment: soil or water
3. Portal of exit
Portal of exit is the route of infectious agent to get out from body of its
house. For example: respiratory tract, GI tact, lesion on the skin, and
mucous membranes.
4. Transmission
Transmission can happen through direct or indirect. Direct transmission is
divided into two types, direct contact (through skin, kiss, sexual, direct
contact with infectious soil or water) and droplet (cough, talk). Indirect
transmission is transmission through air particle, and vector.
5. Portal of entry
Infectious agent goes in to the host’s body through portal of entry. This
portal supplies the agent to multiply and produce toxin.
6. Susceptible host
Host is human or another organism which get infected with infectious
agent. Susceptible host are influenced by general factor, genetic, and
immunity.
The body give response to infection with inflammation. Inflammation is
body respond because of infection, tissue destruction, and other dangerous
condition. Inflammation aims to eliminate harmful stimuli and also heal
damaged tissue. (Ahmad Afsar, 2011).
Infection occurs progressively and the severity of the infection depends
on the level of infection, pathogenicity of microorganisms and host
susceptibility. With the right treatment process, it will minimize the spread
and minimize disease. The development of the infection affects the level of
nursing care provided. Various components of the immune system provide an
excellent complex network of mechanisms, which, if intact, function to
defend the body against foreign microorganisms and malignant cells. In some
circumstances, the components of both specific and nonspecific responses can
fail and this results in damage to the host's defenses. People who get
infections caused by deficiencies in defense in terms of their host are called

8
weakened hosts. Whereas people with major damage related to specific
immune responses are called immunosuppressed hosts.
Inflammation can be characterized by redness (rubor), swelling (tumor),
heat (heat), dolor and loss of tissue function. These signs occur due to the
response of the immune system, blood vessels and inflammatory cells to the
lesion received.
2.2. Tuberculosis
Tuberculosis (TB) is a chronic granulomatous infectious disease that has
been known for centuries and is most often caused by Mycobacterium
tuberculosis. Most of the TB germs attack the lungs, 85% of all TB cases are
pulmonary TB, the rest (15%) attack other organs ranging from the skin,
bones, internal organs such as the kidneys, intestines, brain, and others
(Icksan and Luhur, 2008). Based on the results of sputum examination,
tuberculosis is divided into: BTA positive pulmonary TB: at least 2 of 3
sputum smear positive specimens, smear negative pulmonary TB: from 3
smear negative specimens, positive chest X-ray (Rani, 2006). Infection in the
lungs and sometimes the surrounding structures, caused by the bacterium
Mycobacterium tuberculosis (Saputra, 2010).
The cause of tuberculosis is the bacterium Mycobacterium tuberculosis.
Mycobacteria are included in the family Mycobacteriaceae and are included
in the order Actinomycetales. Mycobacterium tuberculosis includes M. bovis,
M. africanum, M. microti, and M. canettii (Zulkoni, 2010).
2.2.1. Hematogenic TB Spread

The most common hematogenous spread is in the form of occult

haematogenic spread. In this way, TB germs spread sporadically and little
by little so that they do not cause clinical symptoms. TB germs will then
reach various organs throughout the body. Organs that are usually targeted
are organs that have good vascularization, such as the brain, bones,
kidneys, and lungs themselves, especially the lung apex or upper lobe of
the lung. In these locations, TB germs will replicate and form germ
colonies before cellular immunity is formed which will limit their growth.
(Werdhani, RA, 2019).

9
 Another form of hematogenous distribution is acute generalized
hematogenic spread. In this form, large amounts of TB germs enter and
circulate in the blood throughout the body. This can cause acute clinical
manifestations of TB disease, called disseminated TB. Disseminated
tuberculosis occurs within 2-6 months after infection occurs. The
emergence of the disease depends on the number and virulence of
circulating TB germs and the frequency of repeated spread. (Stefanie,
2017)
A rare form of hematogenous spread is protracted hematogenic
spread. This spread occurs when focus on the vascular wall breaks and
spreads throughout the body, causing TB bacteria to enter and spread in
the blood. This can be repeated and clinically difficult to distinguish from
tuberculosis due to acute generalized hematogenic spread. (UDINUS)
2.2.2. Spread of TB in the lung

Tuberculosis has been known to man for many centuries and is

caused by the bacillus Mycobacterium tuberculosis, a member of the
mycobacterium family. It has made a re-emergence in recent decades to
such an extent that in 1993 the World Health Organization declared
tuberculosis as a ‘global emergency’. The mode of transmission in humans
is by inhalation of infected aerosol droplets, and usually causes disease in
the lungs. However, any system in the body may be affected. (Jordan T.S.,
et al., 2010)
When a tuberculosis infection arises becomes active, around 90%
always involve the lungs. Symptoms include chest pain and prolonged
coughing. About 25% of sufferers do not show any symptoms (so called
"asymptomatic"). Sometimes, sufferers experience a slight coughing up of
blood. In rare cases, the infection can erode into the pulmonary artery, and
cause severe bleeding called Rasmussen's aneurysm. Tuberculosis can also
develop into a chronic disease and cause extensive scarring in the upper
lobes of the lungs. The upper lungs are most commonly infected. The
reason is not yet clear. This may be because the upper lungs get more air

10
flow or it could be due to poor lymph drainage in the upper lung. (Lawn,
SD ,2011).
Lung is a port d’entre more than 98% of cases of TB infection.
Because of their very small size, TB germs in inhaled tiny splashes
(droplet nuclei) can reach the alveoli. The entry of TB germs will soon be
overcome by non-specific immunological mechanisms. Alveolar
macrophages will phagocyte TB germs and are usually able to destroy
most TB germs. However, in a small number of cases, macrophages are
unable to destroy TB germs and they will replicate in macrophages. TB
bacteria in macrophages that continue to multiply, will eventually form a
colony in that place. The first location of a TB colony in lung tissue is
called the GOHN Primary Focus.
From the primary focus, TB germs spread through the lymph
channels to the regional lymph glands, the lymph glands that have lymph
channels to the primary focus location. This spread causes inflammation in
the lymphatic ducts (lymphangitis) and in the affected lymph nodes
(lymphadenitis). If the primary focus is located in the lower or middle lung
lobe, the lymph glands that will be involved are the parahilus lymph
glands, whereas if the primary focus is located in the lung apex, the
paratracheal gland will be involved. The primary complex is a
combination of primary focus, enlarged regional lymph nodes
(lymphadenitis) and inflamed lymphatic ducts (lymphangitis). (Nandi, B.,
& Behar, S. M., 2011)
The time needed from the entry of TB germs to the formation of
the primary complex in full is called the TB incubation period. This is
different from the understanding of the incubation period in other
infectious processes, namely the time required from the entry of germs to
the onset of symptoms of the disease. The TB incubation period usually
lasts for 4-8 weeks with a time span of 2-12 weeks. During the incubation
period, germs grow to reach 103-104, which is an amount sufficient to
stimulate the response of cellular immunity. (Sasindran, S. J., &Torrelles,
J. B. 2011)

11
 During the initial weeks of the infection process, there is a
logarithmic growth of TB germs so that the body's tissues, which were not
sensitized to tuberculin initially, develop sensitivity. At the time of the
formation of this primary complex, primary TB infection was declared to
have occurred. This is marked by the formation of hypersensitivity to
tuberculoproteins, namely the emergence of a positive response to the
tuberculin test. During the incubation period, the tuberculin test was still
negative. After the primary complex is formed, the body's entire immunity
to TB has formed. In most individuals with a functioning immune system,
as the cellular immune system develops, the proliferation of TB germs
stops. However, a small number of TB germs can still live in granulomas.
When cellular immunity has formed, new TB germs that enter the alveoli
will be destroyed immediately.
After cellular immunity has formed, the primary focus in the lung
tissue usually undergoes complete resolution to form fibrosis or
calcification after experiencing necrosis of the tree and encapsulation.
Regional lymph nodes will also experience fibrosis and encapsulation, but
the cure is usually not as perfect as the primary focus in the lung tissue. TB
germs can stay alive and stay for years in this gland.
Primary complexes can also experience complications.
Complications that occur can be caused by lung focus or in the regional
lymph nodes. The primary focus in the lung can be enlarged and cause
pneumonitis or focal pleurisy. If severe necrosis occurs, the middle part of
the lesion will melt and come out through the bronchus leaving a cavity in
the lung tissue (cavity). The hilum lymph nodes or paratracheal which
initially normal size at the beginning of the infection, will be enlarged due
to a continuing inflammatory reaction. Bronchial can be disturbed. Partial
obstruction of the bronchi due to external pressure can cause ateletaxis.
Glands that experience inflammation and necrosis can cause damage and
erosion of the bronchial wall, causing endobronchial TB or forming
fistulas. The mass of the lentil can cause complete obstruction of the

12
bronchi, causing a combination of pneumonitis and ateletaxis, which is
often referred to as a collapsed-consolidated segmental lesion.
During the incubation period, before the formation of cellular
immunity, lymphogenic and hematogenous spread can occur. On
lymphogenous spread, germs spread to the regional lymph glands to form
a primary complex. Whereas in hematogenous spread, TB germs enter the
blood circulation and spread throughout the body. The presence of
hematogenous spread is what causes TB is called a systemic disease.
(Walzl, G., et al., 2011)
2.2.3. Pathogenesis of TBC

Infection occurs when a person inhales droplet nucleus 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. Further details about pathogenesis of latent
tuberculosis infection (LTBI) and TB disease are:
1. Droplet nuclei containing tubercle bacilli are inhaled, enter the
lungs, and travel to the alveoli.
2. Tubercle bacilli multiply in the alveoli.
3. 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).
4. Within 2 to 8 weeks, special immune cells called macrophages
ingest and surround the tubercle bacilli. The cells form a barrier

13
 shell, called a granuloma, that keeps the bacilli contained and
under control (LTBI).
5. If 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.

2.2.4. Clinical symptoms of TBC

Tuberculosis can affect every aspect in our body and have so many
clinical symptoms in their body. There are some general symptoms that
occur in the Tuberculosis-infected patients, like weight loss, Fever and
sweating which usually occur in the night, loss of appetite, and feeling
hard to breathe. Besides the general symptoms, there are some respiratory
TB symptoms like coughing with Sputum, Tiredness, Arrhythmia
(irregular heart rhytm), and Hoarseness.
Despite the general and respiratory TB clinical symptoms, there are
some symptoms can be found in tuberculosis-infected patients. According
to Sharma, D. and Sharkar, D. (2014), If a patient has any of the following
traits, we can consider him/her a “Tuberculosis-infected Suspect”. The
traits are cough for over 3 weeks, Haemoptysis (bleeding cough), and have
a pain in the chest for over 3 weeks. All of the symptoms can be due to
some other diseases but sputum must be tested if any of the symptoms are
present because cough and sputum is very common everywhere and it
could be due to acute respiratory infections that lasts only a week or two.
TB usually develops as a necrotizing pneumonia and disseminates
widely in the bodies of infants and immunosuppressed people.
Immunosuppressed people infected with M. Tuberculosis (MTB) for the
first time develop caseating granulomas that contain the organisms. post
primary TB begins by reactivation of dormant MTB or new infection from
the environment. It starts with infection of alveolar cells in persons who
maintain effective immunity to protect the entire rest of their bodies. The
lesions develop as an endogenous lipid pneumonia. If they do not regress,
the lesions undergo necrosis to produce a caseous pneumonia that may

14
become a fragment and be expelled from cough to leave oral cavity or
remain as a mass that induces granulomas and fibrocaseous disease.
(Hunter, R.L., et al, 2014)

2.2.5. TBC Examination

1. Culture specimen
Examination with the media is more sensitive than microscopic
examination because it can compare 10-1000 mycobacteria / ml compared
to microscopic examination which can support positive results if it has
reached 5,000 mycobacteria / ml. (Frieden TR,2004)
 SPUTUM (EXPECTORATED)
Three early morning specimens obtained on different days
should be submitted. A volume of 5 to 10 mL is adequate and there is
no advantage in collecting a larger volume. The sample should contain
recently discharged material from the bronchial tree with minimal
saliva content.
 SPUTUM (INDUCED)
If the patient has difficulty producing a sputum specimen, then
induction should be considered. Sputum production may be induced
by the inhalation of a warm aerosol of sterile 5-10% sodium chloride
in water produced by a nebulizer.
The specimen should be clearly marked "INDUCED" on the
request slip since nebulized sputa is watery in consistency and could
be mistaken for saliva.
2. Ziehl-Nielsen staining
 Methods
This research is a descriptive experimental research that is to
find Mycobacterium Tuberculosis germs from cough patients ≥ 2
weeks in the BLU Internal Medicine clinic. Prof. Dr. R.D Kandou
Manado by using BTA examination conducted in November 2012 to

15
December 2012 at the Health Support Center of the North Sulawesi
Provincial Health Office.
 Tools and materials
Tools: sputum bottles, loop / loop, slide glass, permanent
markers, preparation racks, gloves, masks, stop watch, lamp spiritus,
alcohol. Ingredients: sputum, carbol fuchsin 0.3% solution, alcoholic
acid solution (HCL alcohol 3%), methylene blue 0.3% solution,
xylol.
 Procedure
1) How to take sputum
a. Give a clear label of the patient's identity on the outside
wall of the sputum pot. Susanti, Kountul, Buntuan; Acid-
Resistant Basil (BTA) Examination in Sputum
b. Sputum taken must come from the trachea or bronchi,
not saliva (saliva).
c. The patient is told to rinse his mouth with water before
removing the sputum.
d. Take a deep breath 2-3 times with each breath strongly.
e. Place the opened sputum pot close to the mouth and
remove the sputum into the pot.
f. Cover the pot tightly by turning the lid.
2) How to make preparations
a. Making preparations
Take a phlegm pot and a glass preparation that has the
same identity as a phlegm pot. Then make the dosage clear,
as follows: Heat the osse over the spiritus flame until it is
red and let it cool then take the sputum spread evenly on the
glass surface of the preparation and hold the osse on the
spirits fire until it is dry and the preparation is left in the
open air. After half dry, make a small circle using a taper
stick then pass the preparation on a spirit’s lamp 3 times to

16
fix and place the preparation on a painting rack to be
colored with Ziehl-Neelson's staining.
b. Staining by the Ziehl-Nelsen method.
The fixed fixation is placed on the staining rack with
sputum smear facing upwards then drop 0.3% carbol
fuchsin solution on the sputum smear until it covers the
entire surface of the preparation until it is heated with fire
spiritus until the steam comes out for 3-5 minutes. Then
rinse with running water slowly until the substance is
removed and then drip with alcoholic acid (HCL alcohol
3%) until the fuchsin red disappears. Continue to rinse with
running water slowly and then drop a solution of methylene
blue 0.3% on the preparation until it covers the entire
surface and let stand 10-20 seconds then rinse with running
water slowly then dry the preparation on a drying rack in
the open air. (The hague, 2009)

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 Chapter III

CONCEPTUAL MAPPING

18
 Chapter IV

DISCUSSION

In the case above, A 61 years old male patient with a height of 165 cm and
weigh 50 kg, who lives in a dense city and work as a miner is suffering from
stomatitis on the tongue for one month that has been handled by administering
mouthwash but it didn’t heal. Further examination found inflated left lymph node.
The patient also informs that he has difficulty to breathe, sweating at night, and
coughing at night. After an additional lab examination using Ziehl-Nielsen
staining test and histopathology test found acid resisting rod in the sputum, the
Histopathology test shows tissue granulation. From all the information gathered it
is suspected that the Ulcer that won’t heal is caused by a systemic Tuberculosis
infection.
The suspicion appears by correlating the living conditions (living in a
dense city and works as a miner) and with the test results mainly by the Ziehl-
Nelsen staining test which found acid resisting rod bacteria from the sputum.
Assuming from the evidence above, the infection started by the patient’s living
condition exposing him to prolonged inhalation of Tuberculosis bacteria allowing
it to enter the alveoli giving the tuberculosis the opportunity to replicate within the
alveoli causing chronic tuberculosis.
Tuberculosis germs in inhaled tiny splashes (droplet nuclei) can reach the
alveoli. The entry of tuberculosis germs will soon be overcome by non-specific
immunological mechanisms. Alveolar macrophages will phagocyte the
tuberculosis germs and are usually able to destroy most Tuberculosis germs.
However, in a small number of cases, macrophages are unable to destroy
tuberculosis germs and they will replicate in macrophages creating colonies called
the Gohn Primary Focus. From the primary focus, Tuberculosis germs spread
through the lymph channels to the regional lymph glands, the lymph glands that
have lymph channels to the primary focus location. This spread causes
inflammation in the lymphatic ducts (lymphangitis) and in the affected lymph
nodes (lymphadenitis). There was found a swollen lymph gland on the left part of

19
the neck as is the clinical symptom from the spread of Tuberculosis through the
lymph channel within the body causing the aforementioned lymph node to enlarge
causing lymphadenitis.
The hilum lymph nodes or paratracheal which initially normal size at the
beginning of the infection, will be enlarged due to a continuing inflammatory
reaction. If those lymph nodes enlarge, the bronchial airway can be disturbed.
Partial obstruction of the bronchi due to external pressure causes Atelectasis hence
a difficulty to breathe.
Hematogenous spread occurred by occult hematogenous spread attacks the
lymph nodes, lowering Lymphocyte productions, putting the patient in an
immunocompromised state. This immunocompromised state causes oral ulcer and
weight loss, decreasing intake and malabsorption of nutrients. Changes in the
body's metabolism causing the process of decreasing muscle mass and fat as a
manifestation of protein energy malnutrition. Oral ulcer can also be caused by the
Tuberculosis, although its rarity lowers the chances and the causes of an oral ulcer
varies from case to case, from this case it is highly suspected that the oral ulcer in
this case is an idiopathic oral ulcer for there is only evidence of an immunology
mediated pathogenesis.

20
 Chapter V

CONCLUSION

5.1. Conclusion
1. Based on the case given as well as the history and clinical symptoms, the
patient suffered from tuberculosis with clinical manifestations of
stomatitis. The disease spreads with several ways which is hematogenous
spread, lymphogenous spread, and paratracheal / pulmonary spread.
2. Tuberculosis is an infection that manifested as oral ulcer, weight loss,
inflamed lymph nodes, and difficulty to breathe.

21
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