REVIEW ARTICLE TUBERCULOSIS: EPIDEMIOLOGY ... - rbrs

JBR–BTR, 2006, 89: 243-250.
REVIEW ARTICLE
TUBERCULOSIS: EPIDEMIOLOGY, MANIFESTATIONS, AND THE VALUE OF
MEDICAL IMAGING IN DIAGNOSIS
A. I. De Backer 1 , K. J. Mortelé 2 , B. L. De Keulenaer 3 , P. M. Parizel 4
Mycobacterial infections have been shown to be increasing in number worldwide, mainly due a global increase in
developing countries, the increased number of patients with HIV infection and AIDS disease worldwide, an increasing
number of elderly patients and the emergence of multidrug resistant tuberculosis. Inhalation is the predominant
pathway of Mycobacterium tuberculosis (M. tuberculosis) infection, making pulmonary tuberculosis the most common
form of tuberculosis.Tuberculosis may arise either from a recent infection with M. tuberculosis, or from the reactivation
of dormant bacilli, years or decades after initial infection. Extrapulmonary tuberculosis mainly results from
reactivation of a tuberculous focus after hematogenous dissemination or lymphogenous spread from a primary, usually
pulmonary focus. Tuberculosis may demonstrate a variety of radiological features depending on the organ site
involved and may mimick other pathologies.The final diagnosis of tuberculous disease mainly depends on the detection
of the causative organism on histopathological examination, culture and polymerase chain reaction-based assay
for mycobacterial DNA on material obtained during bronchoscopic washings, fine needle aspiration cytology (FNAC)
or biopsy.
Key-word: Tuberculosis.
Tuberculosis, a disease caused by
M. tuberculosis, has been recorded
in history since the Greco-Roman
and Egyptian civilizations, with evidence
of spinal tuberculosis being
recorded as long ago as 3400 BC.
Ancient Indian scriptures also mention
this disease (1), with the first
known description of tuberculous
spondylitis being written in Sanskrit
sometime between 1500 and
700 BC. However, the modern name
of the disease has been attributed to
Laennec in the 1800s (2).
It has been postulated that
M. tuberculosis existed as an unimportant
pathogen to man until the
coming of the industrial revolution
(3). With resulting urbanisation
and propinquity of living, a new epidemic,
described as ‘a great white
plague’, evolved. In the newly industrialised
countries, the incidence of
tuberculosis probably increased
sharply from the mid 1700s with
subsequent pandemic spread
throughout Western Europe over the
next century and a peak incidence
around 1800 (4). Migration probably
resulted in spread to the United
States, central Africa and also to
South and South-east Asia. As
recently as 1950 tuberculosis has
affected previously completely uninfected
and, therefore, non-immune
populations, such as the Inuit
Eskimos of Northern Canada and
the natives of the highlands of
Papua New Guinea (5, 6).
It has been stated that as tuberculosis
moves through a nonimmune
population, natural selection would
eventually resulted in a resistant
population and subsequent gradually
decline of the disease pandemic.
In most persons, infection with M.
tuberculosis is initially contained by
host defences, and the infection
remains latent. However, latent
tuberculous infection has the potential
to develop into tuberculosis at
any time, and persons with active
tuberculosis become sources of
new infections (7).
Today, tuberculosis remains
endemic in most of the developing
countries. In common with many
other developed countries, Belgium
faces a resurgence of tuberculosis.
After declining for more than a century,
notification rates began to
increase in the mid 1980s and the
long-term downward trend in mortality
also shows signs of levelling
off (8). Several factors may have
contributed to these trends, includ-
From: 1. Department of Radiology, General Hospital Sint-Lucas, Ghent, Belgium, 2.
Department of Radiology, Division of Abdominal Imaging and Intervention, Brigham
and Women’s Hospital, Harvard Medical School, Boston, USA, 3. Intensive Care Unit,
Royal Darwin Hospital, Rocklands, Northern Territory, Australia, 4. Department of
Radiology, Universitair Ziekenhuis Antwerpen, Edegem, Belgium.
Address for correspondence: Dr A. I. De Backer, M.D., PhD, Department of Radiology,
General Hospital Sint-Lucas, Groenebriel 1, B-9000 Ghent, Belgium. E-mail:
adelard.debacker@azstlucas.be.
ing immigration from countries with
a high prevalence and the epidemic
of HIV and AIDS. In addition, other
underlying diseases (diabetes mellitus,
chronic renal failure, chronic
obstructive pulmonary disease, liver
cirrhosis, leukemias and lymphomas)
and numerous sociological
factors contributed to the re-emergence
of tuberculosis: a growing
elderly population; overcrowded
prisons; poor living facilities; poor
nutrition status, alcohol and drug
abuse; persons in long-term care
facilities and homelessness (9, 10).
Among health care workers, the risk
of occupational tuberculosis varies
among and within institutions, but
workers involved in autopsies and
cough-inducing procedures seem to
be at higher risk (11). Finally, it is
known that immigrants visiting their
country of origin can “bring back”
tuberculosis on their return (12).
Tuberculosis may arise in two different
ways: either from a recent
infection with M. tuberculosis; or
from the reactivation of dormant
tubercle bacilli years or decades
after initial infection resulting in
tuberculous disease. As a consequence,
the present level of tuberculosis
comprises both individuals
with “new” exogenous infections
and those with a reactivation of
“old” endogenous disease. The
annual risk of developing pulmonary
tuberculosis following a
recent primary infection is estimated
to be 300 times greater than the
risk of disease from endogenous
reactivation (13). However, older

244 JBR–BTR, 2006, 89 (5)
people having lived through a period
of high tuberculosis incidence
are very likely to have been infected
with M. tuberculosis and now comprise
a growing population group.
In contrast, younger people who
have acquired primary infections
have done so during a period of
much lower incidence and consequently
comprise a smaller subgroup.
Therefore, it has been stated
that disease in the elderly largely
consists of endogenous reactivation
whilst most tuberculosis in younger
people is the result of new exogenous
infection (13).
HIV/AIDS and tuberculosis
It is well established that the
impairment of the immune system
as a result of human immunodeficiency
virus (HIV) infection predisposes
to the development of tuberculosis
and the disease is now
regarded as a “sentinel” manifestation
of the progression from HIV to
AIDS (14-16). The specific targeting
of the CD4 helper cells by the HIV
carries a greater risk of endogenous
reactivation of any latent tuberculous
infection. However, in patients
infected with HIV, opportunistic
infection with M. tuberculosis most
commonly occurs as a result of
exogenous infection (15). The risk of
developing progressive primary
tuberculosis within the first year in
HIV-infected persons is almost 30%
in contrast with the 3% risk of the
non-HIV-infected persons (17).
Infection with M. tuberculosis has
been reported as one of the most
pathogenic of the HIV/AIDS opportunistic
infections (15). Foley et al.
(18) described an increase in the
proportion of tuberculous patients
infected with HIV whilst the total
number of TB notifications remains
largely unchanged and suggested a
direction of causality from the wider
population to the AIDS group.
Tuberculosis as the primary cause of
death has also been reported in
patients suffering from AIDS and
tuberculosis (19, 20).
It is unlikely that HIV will directly
cause a rise in tuberculous rates in
the indigenous population of the
developed world because the incidence
of infection with tuberculosis
amongst the younger population,
which is the one most at risk of
acquiring HIV, is low. However, in
the developing world with a high
prevalence of infection with tuberculosis
in the young adult population,
AIDS-related tuberculosis may
increase dramatically over the next
decade (21). It is likely that the high
and rising rates of tuberculosis in
many developing countries with a
high HIV prevalence will indirectly
make an impact on developing
countries as long as rates of tuberculosis
amongst migrants to the
developed world remain high or
increase further (3). During the past
15 years, alongside the dramatic
rise in HIV, Africa has experienced a
concomitant increase in the tuberculosis
rate (18). In the United
states, HIV infection has also been
implicated in the rapid increase in
tuberculosis notifications or young
men (18). The extent to which HIV is
implicated in the resurgence of
tuberculosis in Belgium will depend
on the overlap between the populations
infected with these two conditions.
However, this overlap seems
to be small.
Manifestations of tuberculosis
Inhalation is the predominant
route of M. tuberculosis infection,
making pulmonary tuberculosis the
commonest form of tuberculous
infection (22). The organism gains
access to the blood stream via the
lymphohematogenous route and
may then affect any organ. The incidence
of extrapulmonary tuberculosis
is increasing, especially because
of HIV (23). In patients infected with
HIV M. tuberculosis usually involves
multiple extrapulmonary sites
including the skeleton, abdominal
organs, and central nervous system.
Tuberculosis may demonstrate a
variety of clinical and radiological
features depending on the organ
site involved and as a consequence
may mimic other pathologies. It is
important to be familiar with the
various radiological features of
tuberculosis to obtain a presumptive
diagnosis as early as possible
(24).
Pulmonary tuberculosis
Pulmonary tuberculosis is classically
divided into primary and postprimary
(reactivation) tuberculosis.
However, a considerable overlap in
the radiological presentations of
those entities may be seen.
Although primary tuberculosis is
the most common form of pulmonary
tuberculosis in infants and
children, it has also been increasingly
encountered in adult patients.
Primary tuberculosis
Primary disease accounts now for
23%-34% of all adult cases of tuber-
culosis (25). Primary pulmonary
infection occurs when an uninfected
person inhales an infectious droplet,
which successfully establishes
infection in a terminal airway or
alveolus (22). The resultant primary
parenchymal (Ghon) focus usually
drains via local lymphatics to the
regional lymph nodes. The combination
of the Ghon focus, local lymphangitis
and regional lymph node
involvement is known as the Ranke
complex. Sometimes, associated
pleural reaction overlying a peripheral
Ghon focus may be present. The
formation of the Ghon complex is
often subclinical and a random
chest radiography following primary
infection is often normal or reveals
only a single component, mostly
hilar adenopathy (Fig. 1) (22).
Disease progression may occur at
the site of the Ghon focus, within
the regional lymph nodes or as a
result of lymphatic drainage with
hematogenous dissemination or
after local penetration across
anatomical boundaries (26). Penetration
may occur into an adjacent
anatomical space or structure, into
an airway with additional intrabronchial
spread or into a blood vessel
with hematogenous dissemination.
Two main types of hematogenous
spread of M. tuberculosis
are differentiated, but dissemination
via the hematogenous route represents
a condition of infinite gradation.
Following dissemination, bacilli
lodge in small capillaries where
they may progress locally and give
rise to further hematogenous
spread. In the other type, disease
progression may result in a caseous
focus eroding into a blood or lymph
vessel (Fig. 2). Except for immunocompromised
patients, the first
type, contrary to the second one,
rarely progresses to disseminated
disease (27).
Primary tuberculosis typically
manifests radiologically as parenchymal
disease, lymphadenopathy,
pleural effusion, miliary disease, or
atelectasis, which may be either
lobar or segmental. Parenchymal
disease in primary tuberculosis
affects the areas of greatest ventilation.
Most commonly, the middle
lobe, the lower lobes, and the anterior
segment of the upper lobes are
involved (11). Atelectasis is usually
the consequence of bronchial
obstruction by an enlarged hilar
adenopathy.
Postprimary tuberculosis
Postprimary tuberculosis usually
results from reactivation of a previ-

Fig. 1. — Ranke complex. Contrast-enhanced chest CT shows
a well-delineated, solitary nodular lesion in the apical segment
of the right lower lobe (straight arrow) and tuberculous right
hilar lymphadenopathy (curved arrow).
ously dormant primary infection in
90% of cases. In a minority of cases,
it may result from the continuation
of primary disease (28). Reinfection
is very rare. Reactivation of mycobacterial
disease is almost exclusively
seen in adolescence and
adulthood. Reactivation occurs as
the result from numerous causes
such as poor nutrition status, neoplasia,
infection or increasing age.
Post-primary tuberculous lesions
show a slow progressive course
resulting in high morbidity and mortality
if not adequately treated (29).
The radiologic features as seen in
postprimary tuberculosis are the
result from a continuous interaction
between the individual patient, with
his own immune status, and M.
tuberculosis (30). The radiologic
features may be classified as parenchymal
disease with cavitation,
airway involvement, and pleural
extension.
Parenchymal pulmonary disease
may show caseous and liquefaction
necrosis and communicate with the
tracheobronchial tree to form cavities
(Fig. 3). A predilection for the
apical or posterior segment of the
upper lobes or the superior segment
of the lower lobes has been reported
(28). Mostly, two or more segments
are involved, and bilateral
upper lobe involvement may also be
noted (11). Most commonly, cavities
occurs within areas of consolidation,
are multiple, and show thick
irregular walls. However, thin and
smooth cavity walls may also be
seen. An air-fluid level within the
cavity is an uncommon finding, and
IMAGING FEATURES OF TUBERCULOSIS — DE BACKER et al 245
may reflect superimposed bacterial
or fungal infection (31).
Bronchogenic spread is a common
complication in postprimary
tuberculosis and represents a chronic
granulomatous infection in which
active organisms spread via airways
after caseous necrosis of bronchial
walls. Endobronchogenic spread is
characterized by multiple, ill-defined
micronodules, distributed in a segmental
or lobar distribution, distant
from the site of the cavity formation
and typically involving the lower
lung zones (30) (Fig. 4). If untreated,
end stage disease may lead to lobar
Fig. 2. — Contrast-enhanced chest CT demonstrates caseous
hilar lymphadenopathy eroding into branches of the right superior
pulmonary vein with subsequent obliteration and dilatation
(curved arrows).
Fig. 3. — Postprimary pulmonary tuberculosis with cavity formation.
CT obtained with lung windowing demonstrates irregular
defined cavities accompanied by mural bronchial wall
thickening and endobronchial spread of tuberculous disease in
both lungs.
or complete lung opacification and
destruction (Fig. 5). However, with
chronic disease, fibroproliferative
lesions composed of nodular opacities
and clearly defined, medium to
coarse reticular areas, may develop.
Most often associated poorly marginated
areas of increased density
may be present (Fig. 6).
A marked fibrotic response is a
common finding after postprimary
tuberculosis and may result in
atelectasis of the upper lobe, retraction
of hilum, compensatory lower
lobe hyperinflation, mediastinal
shift towards the fibrotic lung and

246 JBR–BTR, 2006, 89 (5)
Fig. 4. — Endobronchial spread of tuberculosis (same patient
as Fig. 3). CT obtained with lung windowing shows severe
changes of bronchiolar dilatation and impaction. Bronchiolar
wall thickening (curved arrow) and mucoid impaction of
contiguous branching bronchioles produce a tree-in-bud
appearance (straight arrow).
Fig. 6. — Chronic tuberculous disease characterized by fibroproliferative
lesions. Nodular opacities, coarse reticular areas
and poorly marginated areas of increased density are present.
apical pleural thickening (30) (Fig. 7).
Central airway involvement in
tuberculosis may be the result of
direct extension from tuberculous
lymph nodes, endobronchial spread
of infection, or lymphatic dissemination
to the airway (32). Bronchial
stenosis may result in segmental or
lobar collapse, lobar hyperinflation,
obstructive pneumonia, or mucoid
impaction. A common complication
of endobronchial tuberculosis con-
sists of bronchiectasis resulting from
pulmonary destruction and fibrosis,
and central bronchostenosis.
Pleural effusions in postprimary
tuberculosis are usually small and
associated with parenchymal disease.
A loculated pleural fluid collection
with parenchymal disease and
cavitation may indicate tuberculous
empyema and air-fluid levels in the
pleural space indicate bronchopleural
fistula.
Fig. 5. — Endobronchial spread of tuberculosis with end
stage disease. CT obtained with mediastinal windowing shows
extensive abnormalities of both lungs with distortion of lung
parenchyma, confluent consolidations, multiple cavities,
pleural thickening and effusions.
Fig. 7. — Lung destruction in postprimary tuberculosis. CT
demonstrates a fibrotic, shrunken left lung with compensatory
overexpansion of the right lung. Bronchiectasis is noted in the
left lung with areas of emphysema and atelectasis. Bilateral
symmetrical interstitial nodules, typical of miliary tuberculosis,
are also present.
Occasionally, pericardial involvement
may be seen with mediastinal
and pulmonary tuberculosis and
may cause calcific pericarditis
(Fig. 8) (33).
Imaging findings of pulmonary
tuberculosis
Chest X-rays
Chest X-rays are effective in
demonstrating airspace disease, the
parenchymal nodule that represents
the Ghon focus, diffuse interstitial
disease and pleural effusions
(Fig. 9A). Revealing the presence of
lymphadenopathy is an important
diagnostic sign. However, chest X-

A
rays have been shown to be insensitive
for the detection of lymphadenopathy
(34). On frontal view,
lymphadenopathy is seen as a lobulated
density occupying the hilum
and obliterating the hilar point.
CT
Despite a high radiation dose and
the need for intravenous contrast
administration, CT has evolved to
the modality of choice for the evaluation
of primary and postprimary
pulmonary tuberculosis (11, 30).
Compared to chest X-ray, CT shows
a higher sensitivity for the demonstration
of tuberculous lymphadenopathy
(34). On contrastenhanced
CT, lymphadenopathy
may appear as circular or ovoid
IMAGING FEATURES OF TUBERCULOSIS — DE BACKER et al 247
Fig. 8. — CT and MRI findings in a patient with postprimary tuberculous pericarditis resulting in calcific pericarditis. A. On CT pericardial
thickening with extensive, coarse calcifications are noted. B. Black blood MR image shows calcifications as areas with low
signal intensities. A localised pericardial fluid collection along the wall of the left ventricle is noted.
A
B
B
lesions showing peripheral
enhancement pattern with low-density
centres, heterogeneous, and
homogeneous enhancement. Calcifications
may be present within
these nodes (35). High-resolution CT
is the imaging technique of choice
for demonstration early parenchymal
disease and early endobronchial
spread of disease. Primary
tuberculosis typically manifests as
air-space consolidation that is
dense, homogeneous, and well
defined (22). Typical findings in early
bronchogenic spread of disease are
2- to 4-mm centrilobular nodules
and sharply marginated linear
branching opacities representing
severe bronchiolar impaction, with
clubbing of distal bronchioles
Fig. 9. — Miliary tuberculosis. A. Chest radiograph shows
fine, discrete nodular areas of increased opacity bilaterally.
B. High-resolution CT obtained with lung windowing demonstrates
numerous fine, discrete nodules bilaterally in a random
distribution.
(“tree-in-bud” appearance) (Fig. 4).
In both primary and postprimary
tuberculosis, acute hematogenous
dissemination of M. tuberculosis
may result in innumerable small
tuberculous granulomas in both
lungs. This miliary disease may be
visible on CT before it become radiographically
apparent (Fig. 9B). At
high-resolution CT, a mixture of
both sharply and poorly defined, 1to
4-mm nodules, are seen in a diffuse,
random distribution often
associated with intra- and interlobular
septal thickening (30). On chest
X-ray, the classic miliary pattern
consist of innumerable micronodular
infiltrates, which are all very similar
and diffusely scattered in both
lungs, especially the lung apices.

248 JBR–BTR, 2006, 89 (5)
Fig. 10. — Exudative tuberculous pleuritis demonstrated on
MRI. Contrast-enhanced T1-weighted image shows a right-sided
pleural effusion with enhancement of both visceral and parietal
pleura.
MRI
The use of MRI for the evaluation
of intrathoracic tuberculous lesions
is limited because of technical
limitations, as well as the limited
availability in countries where
tuberculosis is endemic. MRI has
been used for the demonstration of
intrathoracic lymphadenopathy and
pleural effusions (36) (Fig. 10).
Extrapulmonary tuberculosis
Although the predominant form
of tuberculosis is pulmonary disease,
infection with M. tuberculosis
may be seen in any organ system.
Extrapulmonary tuberculosis mainly
results from hematogenous dissemination
or lymphogenous spread
from a primary, usually a pulmonary,
focus. This hematogenous
spread may occur years before the
onset of progressive tuberculosis,
as foci of latent infection may lie
dormant before reactivation
occurs (37). The precise incidence of
extrapulmonary tuberculosis has
not been determined, but an
increasing incidence has been noted
both in developing countries and in
developed countries since the mid-
1980s (38). Especially in patients
infected with HIV an increased
prevalence of extrapulmonary
tuberculosis has been reported (39).
A
B
In these patients multiple extrapulmonary
sites are often involved (11).
Other factors that have contributed
to the increased prevalence of extra-
Fig. 1. — MRI findings of tuberculosis of the central nervous
system, characterized by solid caseating granuloma. A. T2weighted
MR image shows the center of the lesions as
hypointense, probably reflecting caseous necrosis. A smooth,
peripheral hyperintense rim and perilesional edema is noted
(arrows). B. Gadolinium-enhanced T1-weighted image demonstrated
strong ringlike peripheral enhancement (arrows). The
inner part of the lesion and surrounding edema shows absence
of enhancement. The center of the lesion corresponds to
caseous necrosis.
pulmonary tuberculosis are the
development of drug-resistant
strains of M. tuberculosis, and aging
of the population (11, 40). Finally,

the more widespread use of crosssectional
imaging modalities may
also explain why extrapulmonary
tuberculosis is more commonly
been seen.
The most common sites of extrapulmonary
tuberculosis consist of
lymphatic, genitourinary, bone and
joint, and central nervous system
involvement followed by peritoneal
and other abdominal organ involvement
(Fig. 11) (39). Recently, many
authors focused on the imaging features
of extrapulmonary tuberculosis
using cross-sectional imaging
methods (11, 37, 41, 42).
Diagnosis of tuberculosis
The radiological manifestations
of tuberculosis depend largely on
whether the host is naïve to the
infecting organism, i.e. primary
tuberculosis, or whether there has
been reactivation or re-exposure,
i.e. post-primary tuberculosis. As
mentioned previously a broad spectrum
of radiographic appearances
has been attributed to mycobacterial
infections.
Infection with M. tuberculosis is
indicated by a significant tuberculin
skin test. However, the tuberculin
skin test is not 100 percent sensitive
for infection with M. tuberculosis,
and even among patients with
proven tuberculosis and no apparent
immunosuppression, 10 to
20 percent will have negative results
on tuberculin skin tests (7).
Therefore, the diagnosis of
mycobacterial infection often
depends on the detection on the
causative organism. Detection of
the organism on microscopy provides
the most immediate confirmation
but requires a relatively high
organism load in the tissue or fluid
being examined. Detection of M.
tuberculosis by culture may take up
to 6 weeks. A rapid confirmation of
the presence, and type, of mycobacterial
organisms, with a low organism
load, may be achieved using
polymerase chain reaction-based
assay for mycobacterial DNA (43).
With pulmonary tuberculosis, the
use of sputum culture requires a
high burden of organisms to confirm
diagnosis (44). Identification of
infection with a lower burden of
organisms may be obtained by
other techniques, such as bronchoscopic
washings and lung biopsy.
Extrapulmonary tuberculosis,
however, produces no pathognomonic
imaging signs, and in
advanced stages may mimic other
disease processes. Although diag-
IMAGING FEATURES OF TUBERCULOSIS — DE BACKER et al 249
nosis depends largely on the clinical
context, ultrasound, CT and MRI are
valuable tools for early diagnosis
and accurate evaluation of extrapulmonary
tuberculosis. When a mass
lesion is present, fine needle aspiration
cytology (FNAC) or biopsy may
provide material for histopathological
examination, polymerase chain
reaction-based assay for mycobacterial
DNA and culture. Today, FNAC
has become the first-line diagnostic
technique that is highly sensitive
and specific in endemic areas,
where the mere presence of epithelioid
cell granuloma indicates tuberculosis
until proven otherwise.
Furthermore, FNAC provides an
easy way for collecting material for
bacteriological examination.
However, FNAC has several limitations,
especially in the absence of
demonstrable acid-fast bacilli. The
presence of granuloma and/or
necrosis in cytology smears could
not be regarded as definite, especially
in non-endemic areas as they
have several other causes.
Therefore, the combined use of
polymerase chain reaction-based
assay for mycobacterial DNA and
FNAC has been shown to result in
increased sensitivity in FNAC negative,
clinically suspicious cases, and
as a consequence, results in a
reduced need for surgical biopsy
(45).
Conclusion
The clinical and radiologic features
of tuberculosis may mimic
those of many pathologic processes.
A positive culture, polymerase
chain-reaction based assay for
mycobacterial DNA or histologic
analysis on specimens obtained
during bronchoscopic washings for
pulmonary lesions and fine needle
aspiration cytology or biopsy for
mass lesions are still required to
reach a firm diagnosis. In the appropriate
clinical setting, recognition of
the spectrum of imaging features of
tuberculosis may guide diagnostic
work-up and may result in earlier
and adequate treatment.
References
1. Duraiswami P.K., Tuli S.M.: Five thousand
years of orthopaedics in India.
Clin Orthop, 1991, 75: 269-280.
2. Dhillon M.S., Tuli S.M.: Osteoarticular
tuberculosis of the foot and ankle.
Foot Ankle Int, 2001, 22: 679-686.
3. Davies P.D.: Tuberculosis and migration.
The Mitchell Lecture, 1994. J R
Coll Physicians Lond, 1995, 29: 113-
118.
4. Grigg E.R.: The arcane of tuberculosis.
Am Rev Tuberc, 1958, 78: 151-172.
5. Grzybowski S., Styblo K., Dorken E.:
Tuberculosis in Eskimos. Tubercle,
1976, 57: S1-58.
6. Wiggley S.C.: Tuberculosis in Papua
New Guinea. In: Proust AJ (ed).
History of tuberculosis in Australia,
New Zealand and Papua New Guinea.
Canberra: Brogla, 1991, 103-118.
7. Jasmer R.M., Nahid P, Hopewell PC
Latent tuberculosis infection. N Engl
J Med, 2002, 347: 1860-1866.
8. Nisar M., Davies P.D.: Current trends
in tuberculosis mortality in England
and Wales. Thorax, 1991, 46: 438-440.
9. Fain O., Lortholary O., Lascaux V., et
al.: Extrapulmonary tuberculosis in
the northeastern suburbs of Paris:
141 cases. Eur J Intern Med, 2000, 11:
145-150.
10. Lauzardo M., Ashkin D.: Phthisiology
at the dawn of the new century.
Chest, 2000, 117: 1455-1473.
11. Van den Brande P., Vanhoenacker F.,
Demedts M.: Tuberculosis at the
beginning of the third millennium:
one disease, three epidemics. Eur
Radiol, 2003, 13: 1767-1770.
12. McCarthy O.R.: Asian immigrant
tuberculosis-the effect of visiting
Asia. Br J Dis Chest, 1984, 78: 248-
253.
13. Canetti G., Sutherland I., Sandova E.:
Endogenous reactivation and exogenous
reinfection. Their relative
importance with regard to the development
of non-primary tuberculosis.
Bull Int Union Tuberc, 1972, 47: 122-
143.
14. Raviglione M., Norain J.P., Kochi A.:
HIV associated tuberculosis in developing
countries: clinical features,
diagnosis and treatment. Bull World
Health Organ, 1992, 70: 515-526.
15. Festenstein F., Grange J.M.: Tuberculosis
and the acquired immune
deficiency syndrome. J Appl Bacteriol,
1991, 71:, 19-30.
16. Watson J.M., Gill O.N.: HIV infection
and tuberculosis. BMJ, 1990, 300: 63-
65.
17. Zumla A., Malon P., Henderson J.,
Grange J.M.: Impact of HIV infection
on tuberculosis. Postgrad Med J,
2000, 76: 259-268.
18. Kochi A.: The global tuberculosis situation
and the new control strategy of
the World Health Organization.
Tubercle, 1991, 72: 1-6.
19. Elender F., Bentham G., Langford I.:
Tuberculosis mortality in England
and Wales during, 1982-1992: its
association with poverty, ethnicity and
AIDS. Soc Sci Med, 1998, 46: 673-681.
20. McCormick A.: Unrecognised HIV
related deaths. Br Med J, 1991, 302:
1365-1367.
21. Sudre P., ten Dam G., Kochi A.:
Tuberculosis: a global overview of
the situation. Bull World Health
Organization, 1992, 70: 149-159.
22. Marais B.J., Gie R.P., Schaaf H.S., et
al.: A proposed radiological classification
of childhood intro-thoracic
tuberculosis. Pediatr Radiol, 2004,
34: 886-894.

250 JBR–BTR, 2006, 89 (5)
23. Andronikou S., Welman C.J.,
Kader E.: The CT features of abdominal
tuberculosis in children. Pediatr
Radiol, 2002, 32: 75-81.
24. Harisinghani M.G., McLoud T.C.,
Shepard J.O., Ko J.P., Shroff M.M.,
Mueller P.R.: Tuberculosis from head
to toe. RadioGraphics, 2000, 20: 449-
470.
25. Miller W.T., Miller W.T. Jr.: Tuberculosis
in the normal host: radiological
findings. Semin Roentgenol,
1993, 28: 109-118.
26. Marais B.J., Gie R.P., Schaaf H.S., et
al.: The natural history of childhood
intra-thoracic tuberculosis: a critical
review of the literature from the prechemotherapy
era. Int J Tuberc Lung
Dis, 2004, 8: 392-402.
27. Barnes B.F., Bloch A.B., Davidson P.T.,
Snider D.E.: Tuberculosis in patients
with human immunodeficiency virus
infection. N Engl J Med, 1991, 324:
1644-1650.
28. Lee K.S., Im J.G.: CT in adults with
tuberculosis of the chest: characteristic
findings and role in management.
Am J Roentgenol, 1995, 164: 1361-
1367.
29. De Backer A.I., Bomans P.,
Mortele K.J., Leijs J.: Fatal lung
destruction due to phthisis. JBR-BTR,
2004, 87: 203.
30. Van Dyck P., Vanhoenacker F.M., Van
den Brande P., De Schepper A.M.:
Imaging of pulmonary tuberculosis.
Eur Radiol, 2003, 13: 1771-1785.
31. Kuhlman J.E., Deutsch J.H.,
Fishman E.K., Siegelman S.S.: CT
features of thoracic mycobacterial
disease. RadioGraphics, 1990, 10:
413-431.
32. Smith L.S., Schillaci R.F., Sarlin R.F.:
Endobronchial tuberculosis. Serial
fiberoptic bronchoscopy and natural
history. Chest, 1987, 91: 644-647.
33. Taillefer R., Lemieux R.J., Picard D.,
Dupras G.: Gallium-67 imaging in
pericarditis secondary to tuberculosis
and histoplasmosis. Clin Nucl
Med, 1981, 6: 413-415.
34. Delacourt C., Mani T.M., Bonnerot V.,
et al.: Computed tomography with a
normal chest radiograph in tuberculous
infection. Arch Dis Child, 1993,
69: 430-432.
35. Andronikou S., Joseph E., Lucas S.,
et al.: CT scanning for the detection
of tuberculous mediastinal and hilar
lymphadenopathy in children.
Pediatr Radiol, 2004, 34: 232-236.
36. Andronikou S., Wiesenthaler N.:
Modern imaging of tuberculosis in
children: thoracix, central nervous
system and abdominal tuberculosis.
Pediatr Radiol, 2004, 34: 861-875.
37. Vanhoenacker F.M., De Backer A.I.,
Op de Beeck B., et al.: Imaging of
gastrointestinal and abdominal
tuberculosis. Eur Radiol, 2004, 14:
E103-115.
38. Mehta J.B., Dutt A., Harvill L.,
Mathews K.M.: Epidemiology of
extrapulmonary tuberculosis: a com-
parative analysis with pre-AIDS era.
Chest, 1991, 99: 1134-1138.
39. Lupatkin H., Brau N., Flomenberg P.,
Simberkoff M.S.: Tuberculous
abscesses in patients with AIDS. Clin
Infect Dis, 1992, 14: 1040-1044.
40. Engin G., Acunas B., Acunas G.,
Tunaci M.: Imaging of extrapulmonary
tuberculosis. RadioGraphics,
2000, 20: 471-488.
41. Bernaerts A., Vanhoenacker F.M.,
Parizel P.M., et al.: Tuberculosis of the
central nervous system: overview of
neuroradiological findings). Eur
Radiol, 2003, 13: 1876-1890.
42. Moore S.L., Rafii M.: Imaging of musculoskeletal
and spinal tuberculosis.
Radiol Clin North Am, 2001, 39: 329-
342.
43. Hidaka E., Honda T., Ueno I.,
Yamasaki Y., Kubo K., Katsuyama T.:
Sensitive identification of mycobacterial
species using PCR-RFLP
on bronchial washings. Am J Respir
Crit Care Med, 2000, 161: 930-934.
44. Albelda S.M., Kern J.A.,
Marinelli D.L., Miller W.T.: Expanding
spectrum of pulmonary disease
caused by nontuberculous mycobacteria.
Radiology, 1985, 157: 289-
296.
45. Aljafari A.S., Khalil E.A., Elsiddig K.E.,
et al.: Diagnosis of tuberculous lymphadenitis
by FNAC, microbiological
methods and PCR: a comparative
study. Cytopathology, 2004, 15: 44-
48.
POSTGRADUAAT RADIOLOGIE VAN DE VLAAMSE UNIVERSITEITEN
PROGRAMMA 2006-2007
28.09.2006 UA Het postoperatieve gewricht
19.10.2006 UG Neuroradiologie
16.11.2006 KUL Urogenitale Radiologie
14.12.2006 VUB Abdomen
18.01.2007 UA Mammografie
08.02.2007 VUB Radioprotectie
19.04.2007 KUL Angio/Interventionele
17.05.2007 UG Thoraxradiologie