Dr. Alaa Elsawy's Guide to Tuberculosis

Dr.alaa elsawy
Chest specialist
3/6/2017 1
TogetherTo Eliminate TB ,Dr.Alaa elsawy .alsawy73@yahoo.com. Mob.01061644815
Egypt,elsenbellaween,daquahlia.elmostashar street.beside altaher mosque

3/6/2017
Egypt,elsenbellaween,daquahlia.elmostashar street.beside altaher mosque 2

3/6/2017

Tuberculosis Is an
Ancient Disease
SpinalTuberculosis
in Egyptian
Mummies
History dates to
1550 – 1080 BC
Identified by
PCR
Egypt,elsenbellaween,daquahlia.elmostashar street.beside altaher mosque 63/6/2017

3/6/2017

Egypt,elsenbellaween,daquahlia.elmostashar street.beside altaher mosque 93/6/2017

PRINCIPLES OFTB CONTROL:
 1-early diagnosis and
active case-finding
 2-how to support
treatment (including
directly observed therapy)
 3-drug resistance
 4-awareness of drug
interactions
 5-contact investigation after
diagnosing an active case
 6-the importance of adhering to
treatment
 7-treatment forTB is free for
everyone
 8-local referral pathways,
including details of who to refer
and how
 9-the role of allied professionals
in awareness-raising, identifying
cases and helping people
complete treatment( ٌّ‫ي‬ِ‫ن‬ْ‫ه‬ِ‫م‬
‫د‬ِ‫ع‬‫سا‬ُ‫م‬ ٌّ‫ي‬ِ‫ح‬ِ‫ص‬
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Exposure toTB
No infection
(70-90%)
Infection
(10-30%)
LatentTB
(90%)
ActiveTB
(10%)
Untreated
Die within 2 years Survive
Treated
Die Cured
Never develop
Active disease
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 One cough can
release 3,000 droplet
nuclei
 One sneeze can
release tens of
thousands of droplet
nuclei
 Millions of tubercle bacilli in lungs (mainly in
cavities)
 Coughing projects droplet nuclei into the air
that contain tubercle bacilli
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 Large droplets
settle to the
ground quickly
 Smaller
droplets form
“droplet
nuclei” of 1–5 µ
in diameter
 Droplet nuclei
can remain
airborne
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 Sharing dishes and utensils
 Using towels and linens
 Handling food
 Sharing cell phones
 Touching computer keyboard
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- Cough (2-3 weeks or more)
- Coughing up blood
- Chest pains
- Fever
- Night sweats
- Feeling weak and tired
- Losing weight without trying
- Decreased or no appetite
- If you haveTB outside the lungs, you may have other
symptoms
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- WHO declaredTB a global emergency 1993
- 1/3 world population are infected
- Major problem with affordable therapy in some
countries
- Issue of generic drug manufacture
- American attack on pharmaceutical factory in
Somalia removed the only source of available
medication
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- 8 million new cases every year
- 1.3 billion infected
- 9 million have active disease
- 2 million die annually
- Sub SaharanAfrica 300/100,000
- Fatality rate - 23%
- Fatality rate (HIV+TB) - >50%
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 *TheWorld Health Organization (WHO)
estimates that each year more than 8 million
new cases of tuberculosis occur and
approximately 3 million persons die from the
disease.
 *Ninety-five percent of tuberculosis cases
occur in developing countries.
 *It is estimated that between 19 and 43% of
the world's population is infected with
Mycobacterium tuberculosis, the bacterium
that causes tuberculosis infection and disease
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 Most cases in the US are due to reactivation,
especially amongst immigrants
 Highest risk of progression to activeTB is
within 2 years of seroconversion
 Increase in incidence in late 1980s-early 90s
largely due to HIV
 Needs to be reported to the health
department
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 • Definite case of tuberculosis. A patient with
Mycobacterium tuberculosis complex identified
from a clinical specimen, either by culture or by
a newer method such as molecular line probe
assay.
 Pulmonary tuberculosis (PTB- lung
parenchyma
 extrapulmonaryTB- ) (mediastinal and/or hilar)
or tuberculous pleural effusion, without
radiographic abnormalities in the lungs -:
pleura, lymph nodes, abdomen, genitourinary
tract, skin, joints and bones, meninges(
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 Those with increased risk of newTB inecftion
Close contacts
Health care workers) Baseline two-step testing should be performed, followed
by annual testing(
 Those with increased risk of reactivation)Generally
need a single test)
High risk all patients should be tested regardless of age)
 HIV infection (any stage of illness)
 Transplant, chemotherapy, or other major immunocompromising condition
 Lymphoma, leukemia, head & neck cancer
 Abnormal chest x-ray with apical fibronodular changes typical of healedTB (not
including granuloma)
 Silicosis
 Renal failure (requiring dialysis)
 Treatment withTNF-alpha inhibitors
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Moderate risk (patients under age 65 should be
tested)
 Diabetes mellitus
 Systemic glucocorticoids (≥15 mg/day for ≥1 month)
Slightly increased risk (patients under age 50
should be tested)
 Underweight (<85 % of ideal body weight); for most
individuals this is equivalent to body mass index (BMI) ≤20.
 Cigarette smoker (1 pack/day)
 Chest x-ray with solitary granuloma
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 High risk (those whose risk for
reactivation is at least six times higher than
normal healthy individuals
 AIDS & HIV
 Transplantation (related to immune-suppressant therapy)
 Silicosis
 Chronic renal failure requiring hemodialysis
 Carcinoma of head and neck
 RecentTB infection (≤2 years)
 Abnormal chest x-ray with apical fibronodular changes
typical of healedTB (not granuloma)
 Tumor necrosis factor (TNF)-alpha inhibitors
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 Moderate risk (those whose risk for
reactivation is three to six times higher
than normal healthy individuals)
 Treatment with glucocorticoids
 Diabetes mellitus (all types)
 Young age when infected (≤4 years)
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 Slightly increased risk (those whose
risk is 1.5 to 3 times higher than normal
healthy individuals)
 Underweight (<85 percent of ideal body
weight); for most individuals this is equivalent
to body mass index (BMI) ≤20.
 Cigarette smoker (1 pack/day)
 Chest x-ray with solitary granuloma
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 Low risk
 Infected person, no known risk factor, normal
chest x-ray ("low risk reactor")
 Very low risk
 Positive booster (two step test) with no other
known risk factor and normal chest x-ray)
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 Aerobic
 Bacillus (rod-shaped)
 Non-spore forming
 Non-motile
 Cell wall – mycolic acid – retains acid fast
stain
 Growth - doubling time of 15-20 hrs.
 3-8 weeks for
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 PPD – purified protein derivative of
tuberculin (antigenic)
 Delayed type hypersensitivity reaction
 PPD may not become “positive” until 3
months after exposure
 Boosting effect
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 PPD >/= 5 mm:
 –HIV patients
 –Recent contacts of someone withTB
 –Fibrotic changes on CXR c/w priorTB
 –Organ transplant recipients
 –Immunosuppressed (includes patients
receiving the equivalent of 15 mg/day or
more of prednisone for one month or more)
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 PPD >/= 10 mm:
 –Recent immigrants (< 5 years) from high
prevalence areas (Eastern Europe, Latin
America, Asia, Africa)
 –IV drug users
 –Residents and employees of high risk facilities
(hospitals, nursing homes, homeless shelters,
prisons)
 –Children < 4 years of age
 –Mycobacteriology lab personnel
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 PPD >/= 10 mm:
 –People with medical conditions that place them
at high risk for activeTB
 Chronic renal failure
 Silicosis
 Leukemias/lymphomas
 Carcinoma of the head/neck or lung
 Weight loss > 10% of ideal body weight
 Gastrectomy/jejunoileal bypass
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 PPD >/= 15 mm:
 –Low risk people
 –Routine tuberculin testing not
recommended for low risk populations
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 False positives:
 –Non-tuberculous mycobacterial infection
 –BCG vaccination
 False negatives:
 –HIV
 –Malnutrition
 –Steroid therapy
 –Recent infection
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 Bacille Calmette-Guerin vaccination:
 Live attenuated mycobacterial strain
derived
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 Causative organism;
 Mycobacterium tuberculosis COMPLEX
 Stained with:
 -Modified gram stain: gram positive.
 -Carbolfuchsin stain: *Cold method(Kynon)
 *Hot(Zeil-Neelson)
 - Fluorescent dyes: rhodamine and auramine
stains. Bacteriology
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 Cultures: - Lowenstein Jensen media: 6-8
weeks.
 -Bactec media: 2-8days. Radiolabelled 14c
labelled palmitic acid
 -Mycobacterial growth indicator tube:
Middbrook broth+o2 sensitive fluroscent
sensor to indicate growth& bacilli can be
identified by Gen Probe method at the
same day of detection.
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 Acid fast stain of sputum
 Sputum AFB culture (culture needed for
drug susceptibility)
 Radiographic imaging (CXR, CT)
 PCR/NAT
 FluidAspiration
 Tissue biopsy – higher yield than fluid
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 chest X-ray, if chest X-ray appearances
suggestTB.then:
 Send multiple respiratory samples (3 deep
cough sputum samples, preferably,including
1 early morning sample) forTB microscopy
and culture
 3 gastric lavages or 3 inductions of sputum in
children and young people, induction of
sputum or bronchoscopy and lavage in adults
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Suspected
site of
disease
imaging
techniques
Specimen Routine test Additional tests
Pulmonary
(adult)
X-rayb
CT thorax
3 respiratory samples:
preferably
spontaneously-produced,
deep cough sputum
samples, otherwise
induced sputum or
bronchoscopy and lavage
preferably 1 early
morning sample
Microscopy
Culture
Histology
Nucleic acid
amplification test
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Suspected
site of
disease
imaging Specimen Routine test Additional tests
(if
it would alter
management
Pulmonary X-ray
CT thorax
3 respiratory samples:
preferably
spontaneously-
produced,
deep cough sputum
samples, otherwise
induced sputum or
gastric lavage
preferably 1 early
morning sample
Microscopy
Culture
Histology
Nucleic acid
amplification
tests (1 per
specimen
type
Interferon-
gamma
release assay
and/
or tuberculin
skin
test (with expert
input)
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 Transmitted by airborne particles 1-5 microns
in size
 Ease of transmission depends on duration
and proximity of contact as well as the
number of bacteria excreted
 Infection can result from only 1-5 bacteria
entering a terminal alveolus
 Only those with active pulmonaryTB are
infectious
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 *M tuberculosis is transmitted via airborne
droplet nuclei that are produced when
persons with pulmonary or laryngealTB
cough, sneeze, speak, or sing .
 * Droplet nuclei may be produced by
aerosol treatments, sputum
induction,aerosolization during
bronchoscopy, and through manipulation
of lesions or processing of tissue or
secretions in the hospital or laboratory.
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 Inhalation -> phagocytosis by alveolar
macrophages
 –Bacterial multiplication occurs intracellularly
 –Lymphatic spread to regional lymph nodes or
hematogenous dissemination
 –Immune response results in granuloma
formation (containment of infection)
 –Cell death in the granuloma results in caseous
necrosis
 –Bacteria can remain dormant in the granuloma
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 Medical conditions that increase risk for
activeTB:
 Chronic renal failure
 Silicosis
 Leukemias/lymphomas
 Carcinoma of the head/neck or lung
 Weight loss > 10% of ideal body weight
 Gastrectomy/jejunoileal bypass
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 Primary pulmonary tuberculosis *The first
infection with tubercle bacillus. Includes
the involvement of the draining lymph
nodes in addition to the initial
lesion(Ghon).
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 Clinical features:
 Majority: symptomless.(specially in young
adults)
 Brief febrile illness.
 Loss of appetite.
 Failure to gain weight in children.
 Cough is not unusual and may mimic
paroxysm of whooping cough.
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 Physical signs:
 •May be normal,
 •Crepitation may be heard.
 •Primary lesion could be heard.
 •Segmental or lobar collapse may occur.
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 Radiological features:
 •Lymphadenoathy: hilar lymph nodes are
most commonly involved rarely
paratracheal.Calciflcation of the nodes may
occur.
 • Pulmonary componant: ( mainly in adults)
segmental or lobar consolidation or
obstructive emphysema.
 •Resolution of radiological shadow 6m-
2ys.
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 Diagnosis: *Vague ill health with history of
contact. * X-ray. *Tuberclin test: is usually
strongly positive. *Sputum and gastric
lavage for direct smear and culture helpful
in 20-25% of cases. * DNA amplification:
PCR.
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 Primary pulmonary tuberculosis Primary
pulmonaryTB typically manifests
radiologically as parenchymal disease,
lymphadenopathy, pleural effusion, miliary
disease, or lobar or segmental atelectasis.
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 No progression
 Healing by fibrosis and calcification
 Ghons complex after undergoing progressive
▪ fibrosis produces radiologically detectable
▪ calcification called as Ranke complex
 Progressive primary tuberculosis
 Primary miliary tuberculosis
 Dissemination to organs like liver, spleen, kidney, ..etc.
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 10-year-old
child with
tuberculosis
, shows
widening of
the right
paratracheal
stripe
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CT show tuberculous nodes that show central areas of low attenuation suggestive
of caseous necrosis and peripheral rim enhancement

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 Small tan-yellow
subpleural granuloma
in the mid-lung field on
the right.
 Over time, the
granulomas decrease in
size and can calcify,
leaving a focal calcified
spot on a chest
radiograph that
suggests remote
granulomatous disease.
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 typical of
primary
tuberculosis in
a child
 Parenchymal
involvement is
more in adults.
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 The combination of
calcific lesions of the
lung and lymph node is
referred to as the “Ranke
complex”
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 Airspace
consolidation is
usually unilateral,
is evident
radiographically
in approximately
70% of children
with primary TB
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Pleural effusion is
usually unilateral and
due to subpleural
infection.
Pleural effusions are
more common in adults
with primary
tuberculosis (40%).
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shows a right upper lobe
airspace opacity adjacent to
the trachea. In addition,
there is
elevation of the minor fissure
(arrows),
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 focal or patchy
heterogeneous
consolidation
involving the
apicoposterior
segments of the
upper lobes and the
superior segments of
the lower lobes
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 Xray showing
cavitatory
consolidation
in right upper
lung zone and
multiple ill-
defined
nodules in
both lungs
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Cavitation and tree in bud sign is indicative of
an active disease process and usually heals as
a linear or fibrotic lesion.
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MiliaryTB refers to
widespread
dissemination ofTB
by hematogenous
spread.
Seen more frequently
in reactivationTB
Seen in pts with
Location
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The characteristic
radiographic and
high resolution CT
findings consist of
innumerable, 1- to
3-mm diameter
nodules randomly
distributed
throughout both
lungs
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calcified nodule
consistent with a
calcified granuloma.
In addition, there is
bilateral apical
pleural thickening
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tuberculous
cavity can be
colonized by
Aspergillus
species
and present as
an
“aspergilloma”
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spherical nodule or a
mass
separated by a
crescent-shaped
area of decreased
opacity or air from
the adjacent cavity
wall
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HRCT shows
traction
bronchiectasis
in
the right upper
lobe
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This case demonstrates
a left pleural effusion with
air-fluid levels consistent
with a hydropneumothorax
caused by the
bronchopleural fistula.
Diagnosis of
hydropneumothorax is
based on the presence of a
pleural effusion
accompanied by an air-fluid
level within the pleural
space.
3/6/2017 92

Empyema may also
communicate
with the bronchial tree by
bronchopleural fistula and
can show
an air fluid level
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Pneumothorax
occurs in
approximately 5
percent of
patients
with postprimary
TB, usually in
severe cavitatory
disease.
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Bacilli can enter the
pleural space from a
juxtapleural
caseating granuloma,
or
via hematogenous
dissemination
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 Post primary pulmonary tuberculosisThe
most important type of tuberculosis
because it is the most frequent and smear
positive sputum is the main source of
infection responsible for the persistence of
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 Source;
 1. Direct progression of the primary lesion.
 2. Reactivation of the quiescent primary or
post primary.
 3. Exogenous infection.
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 Predisposing factors for reactivation:
 1. Malnutrition. 2. Poor housing and
overcrowding. 3. Steroid and other
immunosuppressive drugs. 4. Alcoholism.
5.Other diseases: HIV malignancy,
lymphomas , Leukaemia,Diabetes.
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 Mainly in middle aged and elderly.
 A-Symptoms:
 1. May be no symptoms, or just mild debility. Gradual
onset of symptoms over weeks or months.
 2. General malaise.
 3. Loss of appetite, loss of weight.
 4. Febrile course.
 5. Night sweating.
 6. Cough with or without sputum.
 7. Sputum could be mucoid, purulent or blood stained.
 8. Could be presented with frank haemoptysis.
 9.Tuberculous pneunonia.
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B-Signs: 1. May be no signs. 2. Pallor,
cachexia. 3. Fever. 4. Post tussive
crepitations on the apices. 5. Signs of
Consolidation. 6. Signs of fibrosis. 7. Signs
of cavitary lesion. 8. Localised wheezes in
endobronchial tuberculosis
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 PostprimaryTuberculosis Postprimary
disease results from reactivation of a
previously dormant primary infection in
90% of cases; in a minority of cases, it
represents continuation of the primary
disease . Postprimary tuberculosis is almost
exclusively a disease of adolescence and
adulthood
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 Cavitary tuberculosis associated with
aspergilloma. Frontal radiograph shows a cavity
in the left upper lobe (black arrow) with a
dependent area of soft-tissue opacity (solid
white arrow).The crescentic area of
hyperlucency (open arrow) represents residual
air in the cavity and is referred to as the air
crescent sign. Axial CT scan shows dependent
soft-tissue aspergilloma (black arrow) within the
cavity (solid white arrow), along with the air
crescent sign (open arrow).
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TUBERCULOUS BRONCHOLITHIASIS. CHEST RADIOGRAPH DEMONSTRATES PARTIAL ATELECTASIS OF THE
RIGHT UPPER LOBE (STRAIGHT ARROW) WITH CALCIFIED HILAR LYMPH NODES BILATERALLY (CURVED
ARROWS). AXIAL CT SCAN DEMONSTRATES EROSION OF THE RIGHT MAIN BRONCHUS (STRAIGHT SOLID
ARROW) BY A CALCIFIEDHILAR LYMPH
NODE (CURVED ARROW). A CALCIFIED PRECARINAL LYMPH NODE IS ALSO NOTED (OPEN ARROW). THE
DIFFERENTIAL DIAGNOSIS FOR MEDIASTINAL LYMPH NODE CALCIFICATION INCLUDES HISTOPLASMOSIS,
SILICOSIS, AND TREATED LYMPHOMA.
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 Tuberculous
bronchostenosis. Axial CT
scan demonstrates
narrowing of the right
main bronchus (arrow).
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 1. Bilateral upper zone fibrotic shadows: with shift of
trachea, mediastinum, distortion of fissures and
diaphragm, and elevation of the pulmonary hila.
 2. Soft confluent shadows of exudative lesion (D.D
pneumonia)
 3 Calcification.
 4. Cavitation.
 5.Tuberculoma.
 6. Hilar and paratracheal lymph node enlargement may be
present.
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 1.Minimal: slight or moderate opacity. No
cavity. Extent not more than space above 2nd
costocondral junction. 2. Moderately
advanced: In one or both lungs. slight or
moderate opacity, extent equivalent to
volume of one lung. Dense confluent shadow
equivalent to one third the volume of one
lung. Diameter of cavities not more than 4 cm.
3. Far advanced: Any lesion>the moderately
advanced
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1) Clinical 2) Plain X-ray. 3) Sputum
Examination: direct smear and culture (very
important). 4) Other samples: Gastric
aspirate, laryngeal swab, fiberoptic specimens
(wash,brush,biopsy),transtracheal spirate.
5 Polymerase chain reaction.) 6)Tuberclin
test: mainly strongly positive 7) OthersWhite
blood cells if normal favour the diagnosis ESR
may be elevated. Normocytic normochromic
anaemia. CT may be useful in detecting small
cavities, or calcification.
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- Uncontrolled haematogenous dissemination
- Progressive primary or reactivation
- Requires impaired immunity thus 50% in
infants, elderly and HIV+
- Clinical course variable; fuminant to subacute
- Non specific presentation; failure to thrive,
aesthenia, night sweats, pyrexia, ARDS
- Difficult to diagnose, 20% post mortem
- Hepatomegaly, ascites, deranged liver
function
- Meningeal disease in 15 – 20%
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 Miliary Disease
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- Ziell Neilsen (acid fast) or Auramine stain.
Others
- Lowenstien Jensen culture
- Automated test - Radiometric culture C14
- PCR and other nucleic acid amplification tests
- Nucleic acid probes for various mycobacteria
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- TB is a notifiable disease
- Contact tracing
-Who was the source?
- Has the current patient been a source?
- Outcomes
- Not infected………….discharge
- Seroconversion but no clinical disease
……..chemo-prophylaxis
- Active disease………..treatment
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RespiratoryTB
- 2 months Rifampicin, Isoniazid, Pyrazinamide,
Ethambutol
- 4 months Rifampicin, Isoniazid
- Pyridoxine
- Now given as combination drugs
- Rifater
- Rifinah
- Sensitivity patterns important
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 More than twenty drugs have been developed
for the treatment ofTB. Most of them were
developed some years ago.The drugs are used
in differing combinations in different
circumstances. For example someTB drugs are
only used for the treatment of new patients who
are very unlikely to have resistance to any of the
TB drugs.There are other drugs that are only
used for the treatment of drug resistantTB.1
There are now starting to be some newTB
drugs, but there is not very much known about
them, and they are still undergoing testing.
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 The five basic or “first line”TB drugs
are:2Isoniazid (H/Inh)Rifampicin (R/Rif) (In
the United States rifampicin is called
rifampin)Pyrazinamide (Z/Pza)Ethambutol
(E/Emb)and Streptomycin (S/Stm)
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 For new patients theWorld Health
Organisation (WHO) recommends that they
should have six months ofTB drug treatment.
This should consist of a two month
“intensive” treatment phase followed by a
four month “continuation” phase.
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 For the two month “intensive”TB drug
treatment phase they should
receive:Isoniazid (H/Inh)with rifampicin
(R/Rif)and pyrazinamide (Z/Pza)and
ethambutol (E/Emb)
followedby Isoniazid (H/Inh)with
rifampicin (R/Rif)
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 Recommendations before May 2016
 Before May 2016 theTB drugs which were
used as treatment for drug resistantTB were
those listed below.They were grouped
according their effectiveness, experience of
use, and drug class, as shown below.
3/6/2017

 All theTB drugs in Group or class 1 are “first
line” drugs. Another “first line” drug is
streptomycin which is with the other
injectable agents in Group 2. All the drugs in
Groups 2 to 5, apart from streptomycin, were
referred to as “second line” or reserveTB
drugs.6
3/6/2017

 The first four groups ofTB drugs listed below
were those that were mainly used for the
treatment of drug resistantTB.The fifth
group ofTB drugs were some drugs that were
unknown in how effective they were in the
treatment ofTB.They could however be tried
when there was no other option.They were
sometimes used in the treatment of totally
drug resistantTB.
3/6/2017

 : First Line Oral Agents
 pyrazinamide (Z/Pza)ethambutol
(E/Emb)rifabutin (Rfb)
3/6/2017

 Groups 2 – 5 Second line drugs (apart from
streptomycin)
 2nd line injectable drugs
 kanamycin (KM) levofloxacin (Lfx) para-
aminosalicylic acid (Pas) clofazimine
(Cfz)amikacin (Amk)moxifloxacin (Mfx)
cycloserine (Dcs) linezolid
(Lzd)capreomycin(Cm) ofloxacin (Ofx)
terizidone (Trd) amoxicillin/clavulanate
(Amx/Civ)streptomycin (S/Stm)
3/6/2017

 Fluroquinolone
 Levofloxacin ,moxifloxacin,ofloxacin
 Oral bacteriostatic 2nd line group
 para-aminosalicylic acid (Pas)
cycloserine (Dcs)
 terizidone (Trd) thionamide
protionamide (Pto)
3/6/2017

 Group A : Fluoroquinolones, Levofloxacin (Lfx), Moxifloxacin
(Mfx), Gatifloxacin (Gfx)

 Group B : Second line injectable agents,Amikacin (Am),
Capreomycin (Cm), Kanamycin (Km), (Streptomycin)
 Group C : Other core second line Agents,
Ethionamide/Prothionamide (Eto/Pto), Cycloserine /Terizidone (Cs
Trd), Linezolid (Lzd), Clofazimine (Cfz)
 Group D : Add-on agents (not part of the core MDR-TB
regimen),) Pyrazinamide, Ethambutol (E), High-dose isoniazid
(Hh) Bedaquiline (Bdq)D2 Delamanid (Dlm),D3 p-aminosalicylic
acid PAS),D3 lmipenem-cilastatin (lpm),D3 Meropenem (Mpm)D3
Amoxicillin-clavulanate (Amx-Clv),D3 (Thioacetazone) (T)
3/6/2017

Dr. Alaa Elsawy's Guide to Tuberculosis

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