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Department of Anatomic Pathology

Faculty of Medicine
Gadjah Mada University

Tuberculosis

is a chronic infection,
potentially of lifelong duration,
caused
by two species of mycobacteria
M.tuberculosis and, rarely,
M.bovis
It was isolated by Robert Koch in 1882
The morbidity and mortality of
tuberculosis are high in developing
countries.

The tubercle bacillus


(M.Tuberculosis) is
aerobie, non-motile,
non-spore-forming,
high in lipid content,
and acid and alcoholfast
It grows slowly ,
It cant tolerate heat,
but It can live in
humid or dry or cold
surroundings.
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A key link of epidemic


The

source of contagious
The route of spread
Peoples of easily affected

Tuberculosis is
transmitted by
airborne
droplet
nuclei(containi
ng tubercle
bacilli )

Many droplet nuclei are


capable off floating in
the
immediate
environment
for
several hours
Large particles may
be
inhaled by a person
breathing the same
air
and impact on the
trachea or wall of the
upper airway

The probability of contact with a


case of TB
The intimacy and duration of
that contact
The degree of infectiouseness of
case
The shared environment of the
contact

tubercle
bacillus

Human immunity
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PULMONARY TUBERCULOSIS

Etiology: mostly
Mycobacterium tb.
Hominis
Pathogenesis:
tipe IV
hypersensitivity

The natural immunity of human to


TB is nonspecific
After
infected or given BCG
vaccine,
human
will
obtain
specific immunity
The immunity of tubercle bacillus
is cell- mediated immunity

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The cellular immunity


develops
within 4 to 8 weeks after infected
with bacillus
Many immunologic cells involve
in the formation of pulmonary
tuberculosis.

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Macrophages: directly phagocytize


TB and processing and presenting
antigens to T lymphocyte
T lymphocytes(CD4+): induce
protection through the production of
lymphokines

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Many lymphokines are involved in


tuberculosis, the interplay of these
cytokines determine the hosts
response for example
IL-1 is related to fever
IL-6 is related to hyperglobulinemia
TNF is related to the killing of
mycobacteria formation of
granolomas
other cytokines including IL-4,IL-5,IL10 can promote humoral immunity

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Genetic factors play a key role

in
innate non immune resistance
to

infection with M. Tuberculosis


These genes may have a role in
determining susceptibility to
tuberculosis

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It refers that there is different


reaction to TB infection between
primary and secondary infection

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Including infiltration, hyperplasia, ulceration


or calcification
These changes happen in different stage of
tuberculosis
When host defense is destroyed and there is
much more bacterias, caseating ulceration
will exist
Otherwise, when host defense is predominant
and there is less bacteria,perhaps hyperplasia
and calcification will happen

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Absorption
Fibrosis
Calcification
Deterioration: enlargement of infected
aeras and appear newer infiltrated
regions or spreading.

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1. Primary pulmonary tuberculosis


(Primary Complex and Bronchial
Lymphnode-Tuberculosis)
2. Milliary Tuberculosis (acute,
subacute and chronic
hematogenous pulmonary
tuberculosis)
3. secondary pulmonary tuberculosis
Infiltrative pulmonary tuberculosis
Chronic fibrocavenous pulmonary
tuberculosis
4. Tuberculous pleuritis
5. Extrapulmonary tuberculosis
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systemic signs:
Most patients present as cases of pulmonary tuberculosis
with fever, weight loss, anorexia, fatigue, night sweats
wasting.

respiratory signs:
Cough may vary from mild to severe, and sputum may be
scant and mucoid or copious and purulent
Hemoptysis may be due to cough of a caseous lesion or
bronchial ulceration
chest pain, tachypnea ect.
Physical signs: nonspecific.

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Allergic reaction to TB
Non-reaction pulmonary tuberculosis

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Chest radiography
Sputum
examination
Tuberculin testing
PCR test to detect
TB
TB antibody testing
bronchoscopy

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White blood count and ESR


The white blood count is usually normal.

In practice the white blood count is only


useful in a minority of cases, When the
patient is less ill and the
radiological
shadowing less extensive the count
is often normal or high normal
ESR is often elevate

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Diagnosis
According to the history, clinical signs, chest X-ray
and some other examinations, we can diagnose TB
A patient with tuberculous pulmonary disease
will come to the physician for one of three
reasons:
(1) Suggestive symptoms
(2) A positive finding on routine tuberculin
testing
(3) A suspicious routine chest roentgenogram

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Generally,

we write the diagnosis


according to the site of TB, clinical
patterns, the result of sputum
examination and the history of
chemotherapy.

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Bronchiectasis may confused with


chronic fibrocavenous pulmonary
tuberculosis. They also have chronic
cough, sputum production and
hemoptysis. Usually we can use chest
x-ray examination and CT scan to
distinguish them.

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Differential Diagnosis

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Cavitary lung abscess often involves the


dorsal segments of the lower lobes and posterior
segments of the upper lobes. Typically lung
abscess causes litt1e in the way of physical
findings, may have a fluid level, and is not
associated with patchy bronchogenic infiltrates.
In contrast, physical findings are prominent
over tuberculous cavities, fluid levels are rare.
And patchy infiltrates elsewhere are the rule.

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Differential Diagnosis

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Acute bacterial pneumonias may


resemble
florid tuberculosis in all
particulars
except for
the
sputum
examination
and
response to
antimicrobial drugs.

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Differential Diagnosis

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Neoplasm may resemble tuberculosis.

As
in an
isolated coin lesion.
An
obstructing
and inconspicuous endobronchial tumor
causing distal chronic
inflammation
or
a caviting neoplastic mass.
(An
irregular cavity
necrotic neoplasm )

wall suggests

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Fever caused by some other


diseases

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Pneumothorax
Bronchiectasis
Empyema
Extrapulmonary expansion
Hemoptysis
Chronic pulmonary heart disease

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Chemotherapy
Support therapy
Surgical therapy

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groups
B groups
C groups
D groups

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the disease in children and implications for


the care of todays child... from a clinicians
view.

H. S. Patterson, M.
D.

Understand, in simple terms, the pathophysiology and clinical course of TB in


children.
Understand the difference between
TB infection and TB disease.
Understand how to make the diagnosis
of TB in a child.

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historical and epidemiologic


perspectives
diagnostic considerations
natural course
mortality/complications
why prophylaxis?

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crowding
decreased access to health care
lower socio-economic status
HIV
? race

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systemic infection
primary infection/disease
progressive primary disease
miliary disease
meningitis
chronic TB (re-activation)

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Inhalation of Infected
Droplet Nuclei

non-specific bronchopneumonia

1) skin test sensitization


2) resistance to exogenous reinfection
3) lympho-hematogenous spread

complete resolution
(rare)

progression

massive necrosis
(rare)

healing with granuloma formation

breakdown with development of


(re-activation)TB

stable

DISEASE
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95% of cases begin


with pulmonary
focus
usually a SINGLE
focus
hypersensitivity
develops 2 to 6
weeks
until then, focus may
grow larger
hypersensitivity
brings caseation
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Tissue Specimens Obtained at Autopsy from the Patient

Jha, A. K. et al. N Engl J Med 2004;350:2399-2404

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8-14 weeks after onset of


TB
usually occult
Mantoux positive during
this phase
body wide seeding occurs
during this phase
bone, kidney, meninges etc.
3% of children with nl CXRs
develop calcifications in lung
apices (SIMON FOCI)
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Jha, A. K. et al. N Engl J Med 2004;350:2399-2404

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lymph nodes draining primary infection


site become involved
lymph node capsule becomes adherent
to bronchial wall

infection can progress to ulceration into the


bronchial wall
bronchial compression occurs with more than
one node at same level
with healing, bronchial constriction/stenosis
can occur

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INFECTION TO ENDO-BRONCHIAL DISEASE

TO STENOSIS
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HEALED PRIMARY INFECTION


SIMON FOCI

CALCIFIED
CALCIFIEDnodes
nodes
and
andperipheral
peripherallesion
lesion
(Ghon
(Ghoncomplex)
complex)

other VISCERAL sites


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USUAL PROGRESSION
OF PRIMARY INFECTION

infection

lympho-hematogenous
spread
healed PRIMARY
infection
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occasional (3.7%) local progression, despite


hypersensitivity (more common in younger
pt)
can be cavitary
can have endo-bronchial spread
similar in appearance to adult type,
reactivation disease
2/3 of cases progress to death in the untreated

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PROGRESSIVE PRIMARY DISEASE


lymph node involvement
cavitation

pleural effusion

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Progressive Primary Disease

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ENDOBRONCHIAL SPREAD
WITH SUBSEQUENT
BRONCHOPNEUMONIA
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Disseminated TB pneumonia

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generalized dissemination through


bloodstream
caseous focus ruptures into blood vessel
growth of tubercle within the blood vessel
may be acute, occult or chronic

uniformly fatal if not treated


rare
usually occurs in the first 4 months after
primary infection

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MILIARY Disease
millet seed
appearance on X-ray
Mantoux positive?
Most children still
have active primary
complex when miliary
disease strikes
most develop
meningitis

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SITES
lymphatics
meninges
pleura
miliary
skeletal
other

Avg. Age
67
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6
5
4

5y
3y
16y
1y
5y

Clin Chest Med 1989, Am. Rev. Resp. Dis, 1990

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Perjalanan penyakit TUBERKULOSIS

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THANK YOU

Bentuk Tbc pada individu yang


belum tersensitisasi (belum
pernah kontak).
Ada 2 bentuk:
1. Afek primer fokus Gohn (lesi
sub-pleural,1-1,5 cm, tuberkel
epiteloid, sel raksasa Langhans,
dan nekrosis kaseosa), di bagian
bawah lobus superior.
2. Komplek primer fokus Gohn
plus penyebaran di hilus
menyebar: pneumonia tbc, atau
disseminasi bronkogenik,
limfogen, hematogen tbc
miliaris meningitis tbc

Pada orang dewasa (reaktivasi, reinfeksi)


Nama lain: Tbc postprimer
Terutama di apex paru (daerah kaya oksigen)
Tuberkel epiteloid dengan perkejuan konglomerasi
kaverne
hemoptisis
Kaverne dianggap sebagai tanda utama tbc sekunder
Kaverne dapat sembuh dengan fibrosis disseminasi
melalui
percabangan trakeobronkial saluran limfe, atau saluran darah

Penyebaran dari tbc paru,


baik
limfogen maupun
hematogen
Menyebar ke organ dan
jaringan: hati dan limpa,
tuba
Fallopii (infertil sekunder,
otak,

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