BONE & JOINT TUBERCULOSIS

Bone and joint tuberculosis is a chronically developed

infection caused by Mycobacterium tuberculosis within bones
and joints.

Etiology & Epidemiology

R. Koch discovered the Mycobacterium tuberculosis in 1882

which has been known ever since as the Koch bacillus (B.K.).
This germ has some specific features:
- it has a strictly aerial metabolism (it is depending on
oxygen)
- it is enveloped in a membrane which is resistant to acid
or alcohol
- it is slowly multiplying in the macrophage cytoplasm.

It may become infectious under some auspicious

circumstances:
- Lack of proper hygiene and nourishment
- Poor biological condition induced by some other infectious
diseases like: measles, scarlet fever, influenza, and whooping
cough.
- Cortisone therapy decreases immunity and leads to
unfavorable general and local development.
- AIDS infection favors tuberculosis (TB)
- Traumatism was found present in 30% of the cases; it is either
relevant for an infection site or favors infection by generating
sites with hemorrhage and necrosis.

It is estimated that at this beginning of the 3rd millennium

we will witness some 4 million deaths / year because of TB and
8 million new diseased patients / year. Obviously, most of
these cases are registered with respiratory TB disease. Only
15% of all TB patients have extra-respiratory disease and in
only 9% we can register bone and joint involvement.
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Pathogenesis

According to Ranke, tuberculosis has a three-stage

development:

1. Initial stage

This is consistent with the penetration and fixation of the

Koch bacillus (B.K.) inside the body.
Penetration will develop in different ways:
- Aerial (97%)
- Digestive (Mycobacterium Bovis)
- Seldom through the conjunctive membranes or the skin
Within the alveolus it will create the primary complex,
consisting of the inoculation chancre, lymphatic trend and
satellite adenitis.
This stage may be clinically invisible, allowing the body
to develop immunity together with tuberculin hyper-sensibility
within 4-6 weeks. A certain number of dormant live bacilli
may still remain and revive under favorable circumstances.

2. Second stage

This may develop immediately or after variable interval.

Hemato-genetic spreading from the primary complex or re-
infection is to be considered at this stage. By urine elimination
of bacilli, urinary tract infections may occur. Visceral and bone
& joint determination can be expected during this
development.

3. Third stage

It is a late development, caused by re-infection or revival

of an older BK site.
Bone and joint infection will be determined by:
- Blood spreading
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- Lymphatic spreading
- Contact with neighboring infection (cold abscess)

Bone and joint TB is always subsequent to primary respiratory

infection that allows blood to carry germs into the bone and
synovia and this is very obvious in children. In adult infection
can be spread from old primary infection (with resting live
bacilli), recent primary infection and seldom from external
source. Only 1/3 of bone and joint BK infections occur in
patients with respiratory disease history.

Bone & joint TB lesion evolution

The disease is manifest as a response to the new presence of

the BK within bone marrow, inside bones or joints. The
primary development occurs inside the marrow, where the BK.
develops the primary metastatic site. This happens in
cancellous or Havers system marrow around small blood
vessels. BK. will cross vessel walls and spread, developing
acute medullitis. Two types of elements will develop:
- Non-specific - vascular neo-formation, exudate, reticular and
macrophage activation
- Specific - creation of the giant follicle (multinucleated, giant,
epithelium-like cells, reticular fibrin, lymphatic cells). This is
consistent with the TB – granuloma.
The lesion progressively develops towards the central marrow
by destroying small blood vessels.
The evolution of the granuloma is accompanied by two
opposing tendencies:
- Granulomatosis – a productive process, proliferation being
induced by irritation;
- Cazeum (the equivalent for pus in TB infection) necrosis - a
destructive process;
The primary metastatic site may have an evolution towards:
-Healing
-Fibrosis
-Secondary complication
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This last possibility allows local spreading of infection within
neighboring area.
There can be:
-Inside evolution for central bone sites;
-External evolution for peripheral sites (cortical or sub-
cortical);
For metaphyseal or epiphyseal locations, the infection site can
be situated close or far from the epiphyseal plate or the
cartilage.

a) Inside bone evolution is present with 2 different types:

- Circumscribed type- a cyst-like isolated tuberculum,
containing cazeum, possibly sequester, granuloma - like tissue;
it is visible on X-ray as a bony cavern.
- Diffuse type – bone decay, with irregular margins and limited
local response; gradually invasive for neighboring tissues.
The repair process determines the para-tubercles osteo-
sclerosis and fibrosis of bone marrow. Spontaneous healing is
exceptional and may happen only in small sites.

b) Out - bone evolution

In this kind of evolution, there is a centrifugal

development of infection towards the periphery of the bone,
either inside or outside of joint.
- Extra-articular way - the granuloma develops in available
space (along blood vessels), reaching the cortical, perforating
it, infecting and destroying the periosteum, which represents
the last obstacle before
developing the cold abscess
within soft tissues.

101. TB within the upper

extremity of the humerus
Cold abscess - results from
gradual peripheral growth and inside cazeum necrosis. Lymph

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drains infected material and induces granuloma in peripheral
positions, while center area fills gradually with cazeum.
Clinically, it is a practically painless tumefaction with a tender
center, without local inflammatory response. It may be difficult
to locate and may readily migrate due to gravity, digging its
way through tissues and cleavage spaces (aponeurosis, blood
vessels, and orifices) thanks to gravity. Under natural
circumstances, it will reach the skin, inducing necrosis from
inside out and festering outside. Such festering sites may be
subjects for common germ infections.
Cold abscess structure comprises:
- The wall - it has 2 layers – one internal, formed by TB
follicles and the presence of BK.
- one external, with granulation tissue,
ensuring spreading to neighboring tissues.
- The content is a yellow –greenish - gray colored liquid, with
debris and cazeum, possibly small sequester. There is no
connection between the size of the cold abscess and that of the
site. It represents a natural way of evacuation for the infection
products and it is diverted by gravity.

Intra - articular way

Invasion of the joint can happen in 3 ways:

- by local proliferation with the infection of the synovial
membrane at the place of it’s insertion on the border of the
cartilage;
- by local cartilage perforation
- by perforation of the local metaphyseal cortical
At this stage, the BK granuloma will have a clinically
noisy development and will produce TB osteo-arthritis,
explaining the secondary involvement of the joints. Joint
infection can be also induced by direct inoculation inside
synovia.

Pathological anatomy

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a) Macroscopic lesions

The initial inoculation can happen within bone or

synovia.
Initial synovial infection will determine TB synovitis. The
synovial membrane appears to be inflamed, thick, red colored,
with white “rice-like” granulation. Sometimes it may be
swollen, pale and rough surfaced, like in rheumatism. Such
lesions first occur in remote pocket areas of the capsule, being
able to infect neighboring bone.
Joint cartilage is normally resistant to BK. Infection, though it
may suffer by ulcer-like secondary lesions in mechanically
stressed areas (Menard) or on the margins (Weber).
Initial bone infection will determine a decay-like lesion,
surrounded by necrosis, edema and fibrosis. Osteoporosis may
accompany this aspect. Invasion of the joint leads to TB
arthritis.
Cold abscess (tuberculoma by Lannelonque) is a result of
tissue destruction because of Koch bacillus.

102. Knee TB involvement

b) Microscopic lesions

There are several characteristic aspects that have to be

mentioned:

1. Inflammatory process with blood vessel dilatation,

lymphocyte infiltration, edema and congestion. Joint aspect
is that of a non-specific synovitis with exceeding fluid.
2. Formation of TB follicle which represents the specific
lesion. The TB follicle consists of epithelial-like and giant
(Langhans) cells, crowned by lymphocytes. Giant
(Langhans) cells have multiple peripheral nuclei (10-80).
They have a central position within follicle and will be
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 replaced by cazeum. Epithelial-like cells have a long or
polygonal appearance, unclearly limited and merged within
a syncytium. Lymphocytes occur after about one week and
have a peripheral distribution.
3. Cazeum necrosis occurs by the 2nd week by coagulation of
matter within the center of the follicle and it is initially
localized, only to spread into the other tissues later. Further
spreading may create an eosinophilic infection site,
bordered with follicles or sclerosis.
4. Pus necrosis is the triggering process of cold abscess
formation. It represents the consequence of tissue
destruction by BK with formation of cavern filling cazeum.

Anatomical pathology according to evolution stage

According to the evolution, Mazabraud describes the following

3 stages: debut, evolution, and repair.
- Debut - TB synovitis; TB osteitis, arthritis.
- Evolution - bone epiphyseal irregularities, metaphyseal
and epiphyseal decay lesions, osteoporosis, sequester.
- synovitis, with all previously described
aspects
- cartilage stripping and necrosis;
- cold abscess from bone and joint drive
outwards and festering
- Repair – the repair process will spontaneously occur after 1-2
years, if specific treatment lacks. When happening, it will
consist of:
- resorbtive / fibrosis tendency for cold abscess and fistula
(festering trail);
- bone repair by condensation (“mourning border”)
- fibrosis in all interested tissues (including capsule,
synovia and inter-bone adherence within joint); live but non-
active bacilli may subside as a potential source for later
relapse.
- anchylose by wide cartilage destruction (long ago seen as
evidence for spontaneous healing);
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Clinical assessment

Symptom aspect will be different according to age, debut and

staging.
It is important to remember that in children tuberculosis is
invading and destructive, whereas in adults its evolution is
remarkably slower and less destructive.

Personal and collateral medical record

- information about life conditions, potential contact and

previous diseases that might decrease body defense
(especially viral respiratory infectious diseases);
- a record of such infections within the social group (school)
or family, that might help establish the infection primary
source and mechanism;
- age proves to be an important factor. TB is a rare event in a
child below 6 months of age.
- multiple determination of TB in small bones (spina ventosa)
is more frequent in younger children, whereas in older ones
bone & joint involvement is more likely;
- TB arthritis is more frequent in teenagers and young adults;
- there is rare but more destructive determination in the
elderly;
- a record of previously observed general signs such as:
tiredness, lack of appetite, perspiration, decrease in body
weight, insomnia, fever.

Debut features

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 - Pain is the most
important debut sign,
bringing the patients to
the hospital. Pain is
slowly occurring,
persistent, more
intense in the evening,
emphasized by effort
and clamed by rest,
not depending on
weather and it is never
completely relieved, as
even in the calm
periods it is still
present as an annoying
sensation.

103. Lower thorax spondilo-discitis (Pott’s disease)

Examination

- Inspection will note particular attitude, muscle contraction,

deformities, as well as abnormal positioning and lower
range of movement in involved joints. In supine / lateral
position, other local details may be noted, along with
paleness and muscle hypotrophy.
- Palpation will show: softening, edema, fluctuence (liquid
like sensation), localized pain, local fever, local muscle
contraction or palsy and local adenitis. Local tissues loose
elasticity, which can be revealed by the Alexandrov sign
(thickened skin fold around superficial joints). Passive and
especially active mobilization are expected to trigger pain
and reveal lack of proper mobility. Swollen ganglia in
inguinal and crural areas (for lesions of the lower limb) and
elbow / axillary ones (for the upper limb lesions) are to be
palpated by comparison to the opposite side.
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- Muscular atrophy – can be assessed by parallel
circumferential measurement.

X-ray assessment

- in children, early occurrence of growth nuclei

- bone demineralization
- unclear joint space
- decreased joint space
- alteration in soft tissue shadow (increased surface in para-
vertebral and capsular shadow);
- bone marginal irregularities

Evolution stage

- signs of general “intoxication”

- emphasized debut-like signs
- hump or limp
- cold abscess
Cold abscess commonly develops without important
inflammatory symptoms, like the warm one. Its local
appearance is that of a soft, mobile tumor, painless and well
limited. It is pear or round shaped and with variable volume.
Cold abscess symptoms can sometimes look like osteo-
arthritis, but there are particular features that clarify things:
- there may be dim burn – like pain and slight local
temperature increase;
- compression upon neighboring nervous structures may
increase pain;
- presence of cold abscess seldom affects general condition;
- local compression can induce functional disturbances,
depending on location (behind pharynx it will induce
dysphagia, psoas sheath involvement will induce thigh
flexion, etc.);
Cold abscess is 3 times dangerous for the patient:

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- toxic effect because of necrotic material resorbtion:
weakening, general condition failure, anemia, insomnia,
paleness, increased white cell count, increased ESR, etc.
- mechanic compression upon other organs: spine cord in
vertebral TB, pharynx, aorta, etc.
- festering and infection with common germs, showing signs
of acute non-specific infection. Festering may have
relapses. Festering displays cold inflammation of the orifice
margins, with elimination of oily or serous, light colored
pus with little blood involvement. Festering can open inside
other organs. Common germ over-infection will trigger
acute inflammatory symptoms and soon require emergency
surgical approach. The outer orifice of the festering trail can
be unique or multiple. It’s exterior aspect can give
information concerning the stage of the TB infection
development:
- prominent, blood - red bud –like formations signify
sequester;
104. Hump in
Pott’s disease

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 - local transparent membrane extension and neighboring
soft tissue involvement – aggravation;
- small pus-emitting buds – long term development;
- retracted scar is equal to healing. Small fragile crust is
visible first, but it comes down and reopens the festering
trail. Soon it closes again – for good – with thin scar
tissue that becomes wider later on.

Specific abnormal (vicious) attitude can be observed in joint

involvement:
- hump is more characteristic in thorax determination, as it
involves more vertebral bodies (in children);
- flexion , adduction and internal rotation in hip
determination;
- flexion, posterior sub - luxation of tibia and external
rotation for knee involvement;
- flexion and ulnar deviation for radio – carpal region;
- flexion and pronation in case of elbow involvement;

x-ray assessment

- bone demineralization (“pencil drawn” bones)

- joint space decrease / disappearance;
- bone decay lesion and irregularities of epiphysis
- loose joint capsule
- abscess shadow
- dim image and lesions of the extremities;

Involution

All symptoms seem to gradually fade away. General condition

gets better, there is increased appetite, pain relief, increasing
body weight. Cold abscess dry up, satellite ganglia shrink,
muscle and joint function is growing. ESR and other blood
tests turn to normal. X-ray turns to condensation images and
bone fusion aspect; the dim image of extremities hardens and
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contrast between bone and soft tissues turns perceptible once
more.

Para-clinical assessment
Biological assessment can offer probability and certainty
arguments. The diagnosis proceeding for bone and joint TB is a
very elaborate one and one has to pass several steps and stages
in order to achieve a clear positive conclusion.
Probability factors that can give us a hint:
- ESR- moderate to relatively high increases (40-90mm/h);
especially useful in assessing
dynamics of the disease;

105. Assessment of intra-

dermal reaction upon TB
infection suspicion

- high leukocyte count - 8-10

000/mmc and neutrophyle
prevailing initially; discrete lymphocyte increase on the way.
- protein metabolism disturbances
- i.d.r. (intra-dermal reaction at 72 hrs.) test represents dermal
response to injection with 10-40 units of PPD – a protein
derivative similar to some of BK components. Unfortunately,
the PPD was last calibrated some 50 years ago and no longer
responds to a very specific revealing of the BK presence. This
is why there are numerous crossed positive reactions with other
pathological conditions of patients, especially viral infections.
The Koch test consists of a similar proceeding to the i.d.r., only
with a larger quantity of PPD (10-40 I.U. compared to 2 – 10
I.U.).
Certainty tests:
- presence of bacilli within secretion from infection site or
synovial liquid examination. There can be typical bacilli (M.
Tuberculosis or Bovis) but also atypical strains (M. Avium, M.
Kansasii, M. Ulcerans, M. Musium, etc.).

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 106. Presence of bacilli in
stained sputum

Three types of bacilli can be

observed during such approach:
active growing bacilli, slow
growing bacilli and dormant
ones. Immediate direct microscopic examination or specific
media culture can be used in order to reveal them. Guinea pig
inoculation is no longer a valuable option, as results are often
inconclusive and come very late (at least three weeks later),
which also makes animal sacrifice doubtfully useful.
- biopsy from satellite ganglia, synovia or bone site, will
reveal the presence of follicle – the one and only specific
histological manifestation for TB infection, especially when we
mention the soft follicle (the one that contains cazeum). The
hard follicle is more difficult to assess, as it may look like the
one in other diseases (leper, Crohn, sarcoidosis, etc.).
- the “quantiferon” test is a brand new system for positive
identification of the presence of BK inside body. We have
inserted this test in the certainty area because it will not fail to
reveal the presence of BK, regardless of its location (lung,
bone, peritoneal, etc.). This allowed CDC Atlanta to impose
this test as a compulsory one for exposed (at risk) groups in the
US. It is simple, trustworthy and comfortable in its application
to large numbers, but it is still too expensive to be extended as
a mass diagnosis method.

Positive diagnosis

A positive diagnosis can be achieved only by assessing all

available information – clinical, biological, x-ray and
histological. As all information will be available on stages,
same thing will happen to the diagnosis.
1st stage demands answer to the following questions:

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- Is joint pain driven by joint elements or just a distant reflex
of another far away lesion?
- Is joint pain accompanied by inflammation? A serious
assessment off past diseases and a correct clinical approach
can give a positive answer.
Once the suspicion of TB is formulated, the patient should be
directed to a specialist. Specialist examination and specific
testing will clarify things: either positive identification (and
immediate setting of the specific treatment) or denial of
diagnosis and the pursue for another, hopefully correct one.
Bone and joint TB diagnosis is consequently based on
several steps:
- anamnesis assessment
- general and local clinical evaluation
- x-ray assessment
- lab tests
- bacteriology tests
- pathological anatomy assessment
The diagnosis proceeding is very important in order to
establish positive or negative decision. There is also legal
responsibility if a case of real TB infection rests undiscovered
and the source – patient goes on infecting other people. Since
there is a need for some type of quantification in order to
standardize the diagnosis and the therapeutical answer, some
assessment criteria have been designed and they have been
awarded points, as follows:

1. Presence of acid – alcohol – resistant bacilli in pathological

products; ............. 3 p
2. Biopsy
a) TB
follicle ...............................................................
....................3 p
b) Non specific lesions
(follicles) ................................................... 1 p
3. Tegument i.d.r. at 10 IU PPD
positive .............................................................. 3 p
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4. Positive conversion of i.d.r. within last 2
years ................................................. 2 p
5. Significant x-ray signs for affected
joints .......................................................... 2 p
6. Positive local clinical
examination ..................................................................... 2 p
7. Confirmed TB
contact ....................................................................................
.... 2 p
8. Non-specific joint x-ray
image ........................................................................... 1 p
9. Significant general clinical
signs ........................................................................ 1 p
10.Significant assessment of joint
fluid ................................................................... 1 p
11.Positive site
response .................................................................................
......... 1 p

Point system evaluation

1 – 2 p - joint disease other than TB;

3 – 4 p - possible TB joint disease, requiring further hospital
investigation;
5 – 6 p - probable TB joint disease, requiring further hospital
confirmation;
over 7 p – certain TB disease;

Evolution

The evolution depends on various factors like:

- Correct diagnosis of the existing stage of the disease;

- how precocious and how adequate the treatment is;
- adequate timing of the various types of treatment;

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Early lesions may heal with convenient preservation of joint
function, whereas older lesions of the bones and joints will heal
by bone destruction and joint stiffness. Lesions may close
imperfectly with follicle confinement. Follicle presence may
delay healing and consequently require surgical extirpation.

Treatment principles

It consists of 4 items:
1. Drug therapy (specific and helper)
2. Orthopedic measures
3. Surgical proceedings
4. Joint rehabilitation

1. Principles of specific drug therapy :

- 3 - 4 drugs association;
- Continuous treatment for 6-12 months;
- SST (strict surveillance treatment) with drugs administrated
2 –3 times a week;
- General and local administration;
- Treatment according to evolution stage;

Anti TB drugs are various:

a) essential -
1. major – Isoniazid (INH); Riphampycin; (active
on live bacilli)
2. associated – Pirazinamid (useful for relapsing
disease with dormant bacilli); Streptomycin;
Etambutol (ETB);
b) spare drugs - Etionamid; Cycloserin; Ciprophloxacin;

Treatment duration will be 6-9 months, sometimes up to 12

months, and will be set by stages:

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- Attack stage –
4 drugs will be used: INH., Riphampycin, ETB and
Pirazinamide or Streptomycin. First three of them will be given
within the first 3 months (morning single dose) and the fourth
will be added starting the 4th month.

- Maintenance stage –
INH and Riphampycin in daily supervised administration from
5th to 9th month.

- Consolidation stage –
INH and Riphampycin twice a week, until the 12th month.

Dosage:
- INH – 5 mg / kg / day
- Riphampycin -10 mg / kg / day
- Pirazinamid – 30 – 35 mg / kg / day
- ETB – 20 - 25 mg / kg / day

Toxic effect of drugs will be assessed at intervals and there are

several criteria for such evaluation:
- transaminasis rate will be followed at 10-14 days, 60 days
and 6 months. Abnormal results must be repeated within 14
days. Treatment must be interrupted when the mentioned
liver enzymes reach 3 times the normal rate;
- eye check-up every 2-3 months when ETB is used;
- hearing assessment when using Streptomycin;
- Pirazinamid use must be accompanied by periodic kidney
check-up;

Drug treatment effect

 Clinical – better general condition; decreasing fever; higher

appetite and weight gaining; decreasing pain and cold
abscess (cold abscess might even disappear). Persistence of
symptoms and cold abscess may be related to improper drug
administration or drug resistance.
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 Para-clinical
ESR is back to normal within weeks. 85-90% of the cases
will prove negative for bacterial test within 3-4 months.
 Radiological
Debut lesions will carry on within the first 2 months.
Reconstruction images will occur afterwards: bone
condensation around the lesion (the “mourning” frame);
osteophytosis; etc. Healing will come with or without
sequels.

Side – effects

INH – Major ones – hepatitis

Minor ones – nerve inflammation; gastric discomfort;
nausea; acne; flushing tegument; blood disturbances;

Riphampycin –
- major reactions - high intensity hypersensitive (allergic)
reactions; patients resuming treatment after some time,
especially by discontinuous therapy, are most likely to be
affected.
- minor reactions – non-hepatic jaundice, especially in
alcoholics. Temporary interruption of the treatment, until
jaundice subsides, is the adequate measure to take.
Headache, feverishness and shivers may accompany
discontinuous treatment, as well as digestive disturbances
(nausea, lack of appetite, vomiting).

Pirazinamid

- major reactions: seldom liver toxic reactions;

- minor reactions: tegument flushing and pricking sensation
2-6 hours after uptake. Digestive trouble and medicine
rejection tendency is also registered. Disagreeable burned
cloth or urine smell may accompany hyper-uric
accumulation, as well as uric arthritis manifestations.

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Etambutol (ETB)

- major reactions: eyesight disturbances that will cease on

treatment interruption;
- minor reactions: digestive discomfort; theratogenetic
reactions during pregnancy;

Streptomycin

- major reactions: hearing and equilibrium disturbances,

dizziness, nistagmus, vomiting;
- minor reactions: paresthesia;

Treatment algorithms for special cases

Pregnancy and motherhood – good action for all TB drugs,

except Streptomycin that can prove toxic for both mother and
child. It should be replaced by ETB. Milking woman can
receive TB drugs and still breastfeed the child without risk.
Child can receive preventive INH treatment and TB vaccine.
Contraceptive drugs may loose 50% of their action when there
is simultaneous Riphampycin uptake.

Liver diseased patients may use INH, ETB and Streptomycin.

The last two can be used during acute hepatitis manifestations,
the third being added afterwards.

Patients with kidney failure may currently use INH, RIF and
PIR (Pirazinamide). STREPTO and ETB are formally banned,
yet they could be employed if kidney functional tests are
available for monitoring.

HIV infected patients can receive the same therapy as common

patients. Care will be taken to use Streptomycin only with all
specific injection precautions.

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Helper Treatment

- Stimulation of natural resistance means of the subject

- ensuring beneficial psychological and social
environment for the patient;
- common use of vitamin complex;
- sun and sea exposure;
- enhanced nutritional uptake;
- recent proof (September 2009)concerning positive
action of HBO (hyperbaric oxygen therapy),
especially in multi-resistant strains of BK (procedure
under development)

Orthopedic means

- 2-4 months bed rest, with proper local immobilization;

- continuous traction for pressure and contraction release;
- plaster cast immobilization in extremely painful cases;
immobilization time has to be as short as possible (30-45
days in adult, 45-60 days in child);

Surgical means

- surgical cleansing of decay after some 3 weeks of drug

treatment; cancellous bone tissue grafting;
- synovectomy after 2-3 months of useless drug treatment in
synovia determination;
- extirpation of tuberculoma and sequester;
- extirpation of cold abscess that did not respond to general
and local treatment;
- surgical removal of sclerosis and grafting;
- osteotomy, arthrodesis and even prosthesis for sequels and
abnormal positioning;

Indication for surgical treatment

- Pott disease with cold abscess;

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- Pott disease with neurological complications:
- If paraplegic symptoms do not subside after 3 months
of treatment;
- If paraplegic development occurs under specific
treatment;
- If paraplegic symptoms are mechanically induced;
- Pott disease with kyphosis :
- Prevention of kyphosis in children (cast and
osteosynthesis);
- Halo-traction test for evolving kyphosis, followed by
similar surgical approach on anterior and posterior
spine;
- For sequel kyphosis surgical approach is rarely
indicated because of straightening accidents
(exceeding tension upon spinal chord);

Specific features in some particular determinations

TB spondylo – disc(itis) [Pott disease]

It seems to be most the frequent bone & joint TB

determination, covering for more than 30% of all cases. In
children it will affect mostly between 3-5 years of age, but it is
frequent at the age of 20-40. Abscess determination of para-
vertebral ganglia may allow lymph seeding, whereas
pulmonary lymph-node abscess can trigger hemato-genetic
inoculation.
According to Menard there are 3 evolution phases:
- debut (invasion ) phase – initial lesion within cancellous
bone tissue; disk unaffected;
- destruction phase – lesion expands from vertebral body
structure towards disk; 3-5 vertebras may be affected in
children and only one in adults; formation of hump by
compression of anterior aspect of vertebral body;
- migration phase – can be extra- rachis or intra-rachis;

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Extra-rachis migration

- within cervical area, the abscess can drive itself forward,

behind the pharynx;
- between neck and dorsal area, abscess may develop within
supra-clavicular area;
- within dorsal area, the abscess is spindle-shaped or sparrow
nest – shaped and can find its way out between the ribs;
- in lumbar area, the abscess is usually driving itself along the
psoas sheath, under the crural arcade and out within Scarpa
triangle (twin pocket abscess), where it can be mistaken for
hernia. Sometimes it will drive itself within adductor
muscle sheath and get as distal as popliteal area.

Intra-rachis migration

- possible migration within spine-chord channel in sub-

occipital area and very rare in cervical area;
- dorsal determination is involving the ligaments;
- in lumbar area, abscess can compress nerve roots inducing
the so called “horse tail” syndrome;
Paraplegic development as neurological complication has been
subject to various classifications: Laiza, Sorrel, Seddon, etc.,
all of which depend mostly by either inflammatory or
mechanical determination.

Clinical development

Pain within dorsal area has an insidious start and will

progressively increase in intensity. Calmed by rest, it is
persistent at night and increased by effort.
Infectious syndrome will accompany pain: fever 38ºC,
paleness, lack of appetite, night sweating. Spine deformity will
become apparent as kyphosis. Cold abscess will be present and
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neurological disorders like disturbed gait or even paraplegia
will soon follow.

X-ray assessment

- early disk shrinking and neighboring bone demineralization

is the most frequent, along with vertebral body erosion;
- mirror disposal of decay (in neighboring bone surfaces) and
irregularities on the vertebral body surface;
- vertebral body decrease in its anterior aspect;
- cold abscess aspect;
- bone marginal densification and osteophytosis reveal
reconstruction (healing tendency);

Other valuable tests

- ESR monitoring
- I.d.r. for PPD
- Scintigraphy may reveal TB sites earlier;
- Bacteriology and histology tests;

There are several clinical types of Pott disease, according to

age:

- in children – rigid spine, several vertebrae involved,

affecting growth centers in vertebral anterior structures,
kyphosis (amplified by disturbed growth);
- in adults – affects only one disk, with slow development
and spontaneous healing by fibrosis;
- in the elderly there is a slower and more discrete
development, with more difficult therapeutical approach;

Dorsal area Pott disease is the most frequent and has the most
typical appearance.

Diagnosis

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Positive diagnosis is based upon:
- clinical arguments –
- biological arguments –
- radiological arguments
- anamnesis arguments –
- bacteriological arguments –

Differential diagnosis is made against:

- growth vertebral epyphisitis (Scheuermann disease)
- congenital block disease
- flat spondylitis
- spondylo-dyscitis determined by : rheumatism, infection,
including Brucellosis, typhus, hydatid, tumors;

Complications

These are mostly related to: kyphosis, lateral deviations, and

complete or incomplete paraplegia.

Treatment

It will be done according to the already mentioned

circumstances.

Sacro-iliac joint TB

Debut is insidious or acute, by brutal lower back pain. Pain is

confined to posterior and superior gluteus area and limping,
discrete in the beginning, will become more and more obvious.
Patient is standing unevenly and sits on one butt. Positive
maneuvers for sacro-iliac joint mechanical stress (Ericsen –
lateral compression upon iliac crest; Verneuil – iliac crest
moving off; Larsey – pushing downwards the shoulders of the
seated patient).
Rectal touch can reveal intra-pelvic abscess.
X-ray evaluation will display decalcification of joint area,
blurred inter-space, decay and sequester, especially in the
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lower joint area. Condensation and bone bridging may occur
during the repair stage.
Treatment will be according to main principles, with surgical
development towards sacro-iliac arthrodesis.

Hip TB

BK is located either within bone or within synovia. Femoral

head and acetabulum are gradually destroyed, even if initial
infection is within synovia. Debut is more intense in children
than adults. Diagnosis is made according to known algorithm
and should be differentiated in kids from arthritis, Perthes
disease or rheumatism. If untreated, the evolution will be
towards ankylosis; if correctly and early treated, lesions are
stabilized with minimal sequels. Treatment is according to
standards and surgical approach will face either arthrodesis of
the hip in extensive lesions or mobilization proceedings (hip
prosthesis) when infection is proved as healed on stiff hip.

There are other types and locations of the TB infection (knee,

ankle, tarsal, shoulder, elbow or radio-carpal). They have some
particular features but treatment will respect the basic
principles.

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